Bootcamp.com Cardiology

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AfraTafreeh.com OUTLINE

Cardiology: Embryology

1. 2.

Embryologic Derivatives Truncus Arteriosus

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A. Physiologic B. Persistent Truncus Arteriosus C. Transposition of Great Vessels

3.

Atrial Septation

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A. Mechanism B. Patent Foramen Ovale C. Atrial Septal Defect

4.

Aortic Arch Derivatives and Pharyngeal Arches

Cardiology: Embryology

Bootcamp.com https://commons.wikimedia.org/wiki/File:2037_Embryonic_Development_of_Heart.jpg

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Sinus venosus à Coronary sinus, posterior portion of right atrium Common cardinal veins à Superior vena cava Umbilical vein à Ligamentum teres hepatis Vitelline veins à Portal circulation and mesenteric veins Truncus arteriosus à Ascending aorta and pulmonary trunk Left and right dorsal aorta à Descending aorta Primitive ventricle à Trabeculated portion of right and left ventricle Primitive atria à Trabeculated portion of right and left atria Bulbus cordis à Smooth portion of the right and left ventricle AfraTafreeh.com Endocardial cushions à Valves and membranous portion of ventricular septum

Heart begins beating during Week 4

Cardiology: Embryology

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Bootcamp.com https://commons.wikimedia.org/wiki/File:Truncus_arteriosus.jpg https://commons.wikimedia.org/wiki/File:D-tga-575px.jpg

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Physiologic: • Neural crest cell migration • Aorta and pulmonary artery partitioned and undergo spiral formation à aorticopulmonary septum constructed Persistent Truncus Arteriosus: • Partial (incomplete) aorticopulmonary septum formation • Mixing of deoxygenated and oxygenated blood • Classic Association: DiGeorge Syndrome Transposition of Great Vessels: • Failed spiraling of aorticopulmonary septum à reversal of pulmonary artery and aorta • Two parallel circuits • Right ventricle à Aorta • Left ventricle à Pulmonary artery • Classic Association: Mothers with diabetes

Cardiology: Embryology

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Step 1: Septum Primum Forms • Forms inferiorly from superior primitive atrium • Foramen primum: opening b/w septum primum + AV cushions Step 2: Foramen and Septum Secundum Form • Foramen Secundum: Forms within septum primum • Septum Secundum: Superior and inferior segment Step 3: Foramen Ovale Closes • Foramen Ovale: Formed by area between septum primum and secundum • ↓ pulmonary vascular resistance, ↑ LAP, ↓ RAP AfraTafreeh.com Patent Foramen Ovale: • Incomplete joining of septum primum and septum secundum • Most patients are asymptomatic • Cryptogenic cerebrovascular accident, paradoxical embolism Atrial Septal Defect: • Secundum-type is most common and tend to be isolated • Primum-type generally associated with additional heart defects • Cryptogenic cerebrovascular accident, paradoxical embolism Ventricular Septal Defects most commonly occur due to defects in the membranous portion of the interventricular septum

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Cardiology: Embryology

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Bootcamp.com https://commons.wikimedia.org/wiki/File:Gray473.png

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First Arch: Maxillary Artery Second Arch: Hyoid and Stapedial Arteries Third Arch: Common Carotid and Proximal Internal Carotid Arteries Left Fourth Arch: Aortic Arch • Classic Pathology: Coarctation of the aorta Right Fourth Arch: Proximal Right Subclavian Artery Left Sixth Arch: Ductus Arteriosus and Proximal Pulmonary Arteries • Classic Pathology: Patent ductus arteriosus Right Sixth Arch: Proximal Pulmonary Arteries

Cardiology: Embryology

Bootcamp.com https://commons.wikimedia.org/wiki/File:Kiemenbogen.jpg

Pharyngeal Arches Segment FirstMandibular Arch

SecondHyoid Arch

Vascular Supply Maxillary Artery

Hyoid and Stapedial Arteries

Cranial Nerve V2 and V3

VII

Important Muscles

Cartilage

-Muscles of mastication -Anterior belly of digastric -Tensor tympani, tensor veli palatini

Meckel’s Cartilage à Mandible, maxilla Zygomatic bone Malleus and incus

-Muscles of facial expression -Posterior belly of digastric -Stylohyoid, stapedius

Reichert’s Cartilage AfraTafreeh.com à Stapes, styloid process Stylohyoid ligament Lesser horn of hyoid

Classic Pathology Treacher Collins Syndrome

Pharyngeal Grooves

1st: Eustachian tube, tympanic cavity, mastoid air cells

1st: External auditory meatus, auditory canal, outer tympanic membrane

2nd: Epithelial lining of palatine tonsils

2nd – 4th: Obliterated in utero

Pierre Robin Syndrome Congenital Pharyngocutaneou s Fistula

3rd: Dorsal à Inferior parathyroid glands 3rd: Ventral à Thymus

Third

Common Carotid and Proximal Internal Carotid Arteries

CN IX

-Stylopharyngeus

à Greater horn of hyoid

Fourth

Aortic Arch (L) R Subclavian (R)

CN X: Superior Laryngeal Nerve

-Cricothyroid -Palatopharyngeus -Levator veli palatini

Superior thyroid cartilage

Coarctation of Aorta

Ductus Arteriosus (L) L Pulmonary Artery (L) R Pulmonary Artery (R)

CN X: Recurrent Laryngeal Branch

Intrinsic muscles of larynx (except Cricothyroid)

Inferior thyroid cartilage Arytenoid, corniculate, and cuneiform cartilage

Patent Ductus Arteriosus

Sixth

Pharyngeal Pouches

4th: Dorsal à Superior parathyroid glands 4th: Ventral à Parafollicular (C cells) of thyroid

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A 57-year-old male with a past medical history of hypertension presents to his primary care physician for hoarseness and dyspnea that has been progressively worsening over the past two months. He has a chronic smoking history ”for as long as he can remember”. He also states that he has been having double vision when leaning forward. During physical examination, auscultation reveals mild end-expiratory wheezing bilaterally over the lung fields. Heart sounds are normal with a regular rhythm. Radial pulses are 2+ and symmetric bilaterally. No thyromegaly is present. Diffuse venous distention is observed in the neck and chest wall. Edema is present diffusely throughout the upper extremities. Fundoscopic examination reveals papilledema bilaterally. Chest radiography is performed. A suspicious mass is identified and highlighted on the imaging study below. Which embryologic derivatives are most closely associated with the structured compressed in this patient?

⚪ A. Truncus arteriosus ⚪ B. Cardinal veins ⚪ C. Endocardial cushions ⚪ D. Right sixth pharyngeal arch ⚪ E. Left fourth pharyngeal arch

Bootcamp.com https://commons.wikimedia.org/wiki/File:SVCCXR.PNG

OUTLINE

Cardiology: Anatomy

1. General Anatomical Overview ● ● 2. ● ● 3. ● ● ● 4. 5. ● ● 6. ● ● 7. ● ● ● 8. 9. ● ● ●

A. Cardiac Atria B. Cardiac Ventricles

Cardiac Silhouette: Chest Radiography A. Cardiac Atria B. Cardiac Ventricles

Axial Imaging: CT and MRI A. Ascending and Descending Aorta B. Pulmonary Trunk C. Cardiac Atria and Ventricles Penetrating Cardiac Injury Cardiac Conduction Anatomy A. Sinoatrial Node B. Atrioventricular Node Radiofrequency Ablation Targets A. Atrial Fibrillation Foci B. Atrial Flutter Foci Coronary Artery Anatomy A. Right Coronary Arteries B. Left Coronary Arteries C. Dominant Coronary Artery Circulation Coronary Sinus Cardiac Catheterization A. Swan-Ganz Catheter B. Coronary Angiography, Percutaneous Coronary Intervention C. Trans-Septal Left Atrial Catheterization

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Cardiology: Anatomy

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https://commons.wikimedia.org/wiki/File:Diagram_of_the_human_heart_(cropped).svg

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Right Atrium: • Right heart border Right Ventricle: • Anterior and inferior heart border Left Atrium: • Posterior border of heart (also minor component of left ventricle) • Clinical Correlation: Enlargement leads to cardiovascular dysphagia • Clinical Correlation: Transesophageal echocardiography Left Ventricle: • Left heart border (also minor component of left atrial appendage)

Cardiology: Anatomy

Bootcamp.com https://commons.wikimedia.org/wiki/File:X-ray_of_cardiac_silhouettes.jpg

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Right Atrium: • Right heart border Right Ventricle: • Anterior and inferior heart border Left Atrium: • Posterior border of heart (also minor component of left ventricle) • Clinical Correlation: Enlargement leads to cardiovascular dysphagia • Clinical Correlation: Transesophageal echocardiography Left Ventricle: • Left heart border (also minor component of left atrial appendage)

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Cardiology: Anatomy

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https://commons.wikimedia.org/wiki/File:Cardiac_mri_slice_bionerd.jpg

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Ascending aorta Descending aorta Pulmonary trunk Atria and Ventricles

https://commons.wikimedia.org/wiki/File:SADDLE_PE.JPG

Cardiology: Anatomy

Bootcamp.com https://commons.wikimedia.org/wiki/File:Surface_projections_of_the_organs_of_the_trunk.png

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Mid-Left Sternal Border 3rd-4th Intercostal Space: • Right ventricle susceptible to injury Left Sternal Border to Mid-Clavicular Line 5th Intercostal Space: • Medial à Left ventricle and left lung susceptible to injury • Lateral à Left lung primarily susceptible to injury

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Cardiology: Anatomy

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https://commons.wikimedia.org/wiki/File:Diagram_of_the_human_heart_(cropped).svg https://commons.wikimedia.org/wiki/File:ConductionsystemoftheheartwithouttheHeart-en.svg

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Sinoatrial Node: • •

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Atrioventricular Node: • •

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Contains specialized pacemaker cells Location: Right atrium along roof (proximity to opening of SVC) Delayed conduction between atria and ventricle Location: Right atrium along interatrial septum (proximity to tricuspid valve and coronary sinus)

Bundle of His Purkinje Fibers

Cardiology: Anatomy

Bootcamp.com https://commons.wikimedia.org/wiki/File:Diagram_of_the_human_heart_(cropped).svg https://commons.wikimedia.org/wiki/File:ConductionsystemoftheheartwithouttheHeart-en.svg

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Atrial Fibrillation Foci: • Left atrial myocardium • Pulmonary vein ostia within left atrium Atrial Flutter Foci: • Area between tricuspid valve and IVC

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Cardiology: Anatomy

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Right Coronary Artery (RCA): • Majority of right-side of heart • Sinoatrial node Left Coronary Artery (LCA): • Majority of left-side of heart • Two major branches: • Left Anterior Descending Artery (LAD)à Anterior 2/3 of interventricular septum, anterolateral papillary muscle, anterior left ventricle • Left Circumflex Artery (LCX) à Posterolateral LA and LV, anterolateral papillary muscle Posterior Descending Artery (PDA): • ~85% R-dominant, 8% L-dominant, 7% co-dominant • Primarily inferior borders of heart • Posterior 1/3 of interventricular septum • Posteromedial papillary muscle

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Cardiology: Anatomy

Bootcamp.com https://commons.wikimedia.org/wiki/File:PPM.png https://commons.wikimedia.org/wiki/File:Gray491.png

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All coronary veins drain into the coronary sinus Location: Left posterior atrioventricular groove Drains directly into the right atrium Embryologic derivative: Sinus venosus Clinical Correlation: Biventricular pacemaker lead placement into LV Clinical Correlation: Dilated in pulmonary hypertension

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Cardiology: Anatomy

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https://commons.wikimedia.org/wiki/File:Pulmonary_artery_catheter_english.JPG https://commons.wikimedia.org/wiki/File:Coronary_Angiography.png

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Swan-Ganz Catheter (Pulmonary Artery Catheter): • • •

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Coronary Angiography, Percutaneous Coronary Intervention (PCI) • •

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Venous catheter Use: Measures right-sided pressures Pulmonary capillary wedge pressure: Surrogate marker for left atrial pressure

Arterial catheter Use: Visualize atherosclerotic lesions and stenosis of coronary vessels

Trans-Septal Left Atrial Catheterization • •

Venous catheter Use: Direct measurement of left atrial pressure and/or ablation of pathogenic foci

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A 25-year-old female presents to the emergency room with dyspnea and palpitations. She states that she believes she may be having a panic-attack. She reports that she was walking her dog when suddenly she began to feel lightheaded and short of breath. She denies any family history of heart disease. Telemetry monitoring reveals an irregularly irregular heart rate of 134/min. Blood pressure is 138/54, respiratory rate is 14/min, blood glucose is 84 mg/dL. Fine tremors are observed in the distal phalanges. Electrocardiogram is performed and shown. Initial labs reveal a significantly decreased thyroid-stimulating hormone level.

AfraTafreeh.com Which of the following locations is likely a source of aberrant electrical foci contributing to this patient’s symptoms?

⚪ A. Cavotricuspid isthmus of right atrium ⚪ B. Superior subendocardial right atrium ⚪ C. Membranous portion of interventricular septum ⚪ D. Left posterior atrioventricular groove ⚪ E. Pulmonary vein ostia of left atrium ⚪ F. Pulmonary artery root of right ventricle

Test Your Knowledge Difficulty: ✪✪✪

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https://commons.wikimedia.org/wiki/File:ECG_Atrial_Fibrillation.jpg

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Cardiology: Vascular System

1. Aorta ● ● ● 2. 3. ● ● ● 4. ● ● 4. ● ● ● 6. ● ●

A. Vascular Structures and Branches B. Ligamentum Arteriosum C. Key Landmarks of the Aorta

Subclavian Steal Syndrome Venous Drainage Obstruction A. Superior Vena Cava Syndrome B. Brachiocephalic Vein Obstruction C. Subclavian and/or Axillary Vein Obstruction Coronary Bypass Grafting A. Internal Thoracic Artery B. Great Saphenous Vein Femoral Access A. NAVEL B. Femoral Arterial Access C. Femoral Venous Access Inferior Vena Cava A. Key Landmarks of the Inferior Vena Cava B. Inferior Vena Cava Filter

Cardiology: Vascular System

Bootcamp.com https://commons.wikimedia.org/wiki/File:Aorta_branches.svg

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Vascular Structures: • Coronary Arteries • Brachiocephalic trunk • Subclavian arteries • Common carotid arteries Ligamentum Arteriosum: • Remnant of ductus arteriosus Key Landmarks: • T12: Descending aorta traverses' diaphragm via aortic hiatus • T12: Celiac trunk • L1: Superior mesenteric artery origin • L3: Inferior mesenteric artery origin • L1-L2: Right and left renal arteries origin • L2: Gonadal arteries origin • L4: Bifurcation into common iliac arteries (at navel)

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Cardiology: Vascular System

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https://commons.wikimedia.org/wiki/File:The_promixal_part_of_left_subclavian_is_blocked_on_left_side_so_no_flow_in_vertebra l_and_to_left_arm-blood_from_right_vertebral_enters_left_vertebral_and_flows_back_to_supply_left_arm_2013-07-05_17-11.jpg

https://commons.wikimedia.org/wiki/File:Angiogram_of_Left_Subclavian_Steal_Syndrome.PNG

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Etiology: Atherosclerosis, Takayasu arteritis, previous thoracic (aortic) surgery Pathophysiology: • Subclavian stenosis à contralateral vertebral artery steal phenomena Presentation: • Ipsilateral limb ischemia • Asymmetric BP between upper extremities • Dizziness, diplopia, syncope • Worsening of symptoms during activity of affected limb Imaging: • Reduced contrast uptake in areas distal to stenosis and ipsilateral vertebral artery

Cardiology: Vascular System

Bootcamp.com https://commons.wikimedia.org/wiki/File:2132_Thoracic_Abdominal_Veins.jpg

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Superior Vena Cava Syndrome • Etiology: Mass lesion (malignancy) or thrombosis (venous catheter) • Edema à bilateral face, bilateral upper extremities • Jugular venous distention Azygos Vein • Headache, ↑ intracranial pressure Right-sided vein Brachiocephalic Venous Obstruction Connects SVC and IVC Alternative pathway for blood to return to right atrium • Etiology: Pancoast tumor or thrombosis (venous catheter) • Edema à Unilateral face, unilateral AfraTafreeh.com upper extremity Subclavian and/or Axillary Venous Obstruction • Edema à Unilateral upper extremity • No facial involvement Inferior Vena Cava Compression • Supine hypotensive syndrome (3rd trimester) Edema à Bilateral lower extremities Fetal hypoxia à improves with repositioning

Cardiology: Vascular System

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https://upload.wikimedia.org/wikipedia/commons/c/c8/2136ab_Lower_Limb_Veins_Anterior_Posterior.jpg https://commons.wikimedia.org/wiki/File:Gray522.png

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Internal Thoracic (Mammary) Artery Great Saphenous Vein • Medial foot, medial malleolus, medial leg and thigh • Joins femoral vein

Cardiology: Vascular System

Bootcamp.com https://commons.wikimedia.org/wiki/File:Gray545.png

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NAVEL (lateral to medial) • Femoral Nerve • Femoral Artery • Femora Vein • Empty • Lymphatics Femoral Arterial Access • At the site of femoral pulsation below inguinal ligament • Coronary angiography, PCI AfraTafreeh.com • Clinical Correlate: If access above inguinal ligament à ↑ risk of retroperitoneal hemorrhage Femoral Venous Access • Medial to the site of femoral pulsation below inguinal ligament • Swan-Ganz catheter • Trans-septal left atrial catheterization

Cardiology: Vascular System

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https://radiopaedia.org/cases/normal-ct-abdomen?lang=us https://commons.wikimedia.org/wiki/File:3D_Medical_Animation_Inferior_Vena_Filter.jpg

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Key Landmarks: • T8: Traverses diaphragm • L5: Formed by right and left iliac veins Inferior Vena Cava Filter • Indication: Failure or contraindication to anticoagulation in the setting of a lower extremity deep venous thrombosis

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A 67-year-old left-handed male is brought to the emergency room by paramedics for 9/10 acute onset chest pain that began during a game a of ping-pong at his senior living facility. The patient states that he has been noncompliant with his statin medication and has not been consistent in checking his blood pressure at home. He reports having chest pain over the past week worsened with rapid left arm movement. His medical history is significant for a myocardial infarction secondary to significant stenosis of the left anterior descending and circumflex arteries and had previously undergone a coronary artery bypass grafting procedure. Physical exam reveals a cool left extremity with a 1+ left radial pulse. The right upper extremity is normal in color with a systolic blood pressure 30 mmHg greater than the left. Cardiovascular surgery is emergently consulted, and a percutaneous revascularization is performed. Retrograde transport of blood through which of the following arteries most likely contributed to this patient’s presentation?

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⚪ A. Right vertebral artery ⚪ B. Left subclavian artery ⚪ C. Left internal carotid artery ⚪ D. Left axillary artery ⚪ E. Grafted internal thoracic artery

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AfraTafreeh.com OUTLINE

Cardiology: Cardiac Parameters of Physiologic Function

1.

Stroke Volume

● ● ● 2. ● ● ● 3. 4. ● ● 6. ● 7. ● ● 8.

A. End-Diastolic Volume B. End-Systolic Volume C. Ejection Fraction Stroke Volume Variables A. Preload B. Afterload C. Contractility

Heart Rate Frank-Starling Mechanism A. Principle and Mechanism B. Frank-Starling Curve Cardiac Output A. Fick-Principle Mean Arterial Pressure A. Total Peripheral Resistance B. Pulse Pressure Coronary Blood Flow and Autoregulation

Cardiology: Cardiac Parameters of Physiologic Function

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End-Diastolic Volume: ~ Preload End-Systolic Volume: ~ 1/Contractility Stroke Volume (SV) = End-diastolic volume (EDV) – End-systolic volume (ESV) Ejection Fraction (EF) = SV / EDV

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Cardiology: Cardiac Parameters of Physiologic Function

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Preload: • ↑ Venous return à ↑ EDV ~ ↑ Preload à ↑ Stroke volume, ↑ Contractility Afterload: • ↑ TPR ~ ↑ Afterload à ↑ ESV à ↓ Stroke volume • Preload compensates in healthy hearts • Afterload has a more dominant effect in heart failure !"#$$%"# & '()*%$ +(,, -#1$*21 • Law of LaPlace: Wall stress = +(,, -.*/01#$$ = +(,, -.*/01#$$ Contractility • ↑ SNS activity à ↑ Contractility à ↓ ESV à ↑ Stroke volume

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SV = EDV - ESV

Cardiology: Cardiac Parameters of Physiologic Function

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Physiologic Mechanism: ↓ Vagal tone à SA Node à ↑ HR Coronary Perfusion: • Left ventricular myocardial perfusion occurs primarily during diastole CO = HR x SV Tachycardia: • Elevated heart rate • ↑ HR à ↓ time of diastole à ↓ ventricular myocardial perfusion, ↓ diastolic filling time à ↓ CO

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Maximal HR = 220 bpm – Age (in years)

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Cardiology: Cardiac Parameters of Physiologic Function

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Principle: • ↑ Preload à ↑ Contractility à ↑ SV Mechanism: • ↑ Venous return • ↑ EDV ~ ↑ Preload • ↑ Myocyte stretch prior to contraction • ↑ Sarcomere length (↑ active tension and velocity of fiber shortening) Frank-Starling Curve: • X-axis: LVEDP (preload, LVEDV, fiber length) • Y-axis: Stroke Volume • Slope of curve: Defined by afterload and contractility • Point along curve: Defined by venous return (preload)

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SV = EDV - ESV

Cardiology: Cardiac Parameters of Physiologic Function

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Cardiac Output = HR x SV Fick Principle à Cardiac Output = Rate of O2 consumption / Arteriovenous O2 difference

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Cardiology: Cardiac Parameters of Physiologic Function

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Total Peripheral Resistance (TPR) = Determined by state of arteriolar resistance Pulse Pressure (PP) = Systolic pressure – Diastolic pressure Mean Arterial Pressure (MAP) = CO x Total peripheral resistance (TPR) Mean Arterial Pressure (MAP) = 1/3 systolic pressure + 2/3 diastolic pressure Mean Arterial Pressure (MAP) = 1/3 PP + Diastolic Pressure

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Cardiology: Cardiac Parameters of Physiologic Function

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Left Ventricular Coronary Blood Flow: ↑ Ventricular diastole Oxygen Extraction: • Significant in myocardial tissues • Coronary sinus à ↑↑↑ deoxygenation • ↑ O2 demand à coronary vasodilation (nitric oxide, adenosine)

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A 57-year-old male presents to the emergency department for a dry cough and dyspnea. He states that over the past seven years he has experienced mild shortness of breath with continued physical exertion, however, over the past week he has suddenly become short of breath at rest. He has a past medical history of poorly controlled hypertension and hyperlipidemia. The patient also admits to a 30-year smoking history. He is afebrile, blood pressure is 102/64, heart rate is 102/min, oxygen saturation is 92% on room air. Auscultation of the heart reveals an S3 heart sound and a faint systolic decrescendo murmur in the axillary region. Lung auscultation is significant for diffuse crackles. There is dullness to percussion over the lung fields. Chest radiography is shown. Which of the following is most consistent with this patient’s presentation?

⚪ A. Elevated systolic aortic pressures ⚪ B. Elevated pulmonary capillary wedge pressure ⚪ C. Depressed left atrial pressure ⚪ D. Depressed pulmonary venous pressure ⚪ E. Unchanged left ventricular diastolic volume

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https://commons.wikimedia.org/wiki/File:Pulmonary_oedema.jpg

OUTLINE

Cardiology: Cardiac Function and Venous Return Curve Physiology

1. Cardiac Function Curves 2. Venous Return Curves 3. Combined Cardiac Function and Venous Return Curves ● A. Steady State ● B. Specific Pathologic Processes

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Cardiology: Cardiac Function and Venous Return Curve Physiology

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Cardiac Function Curve: • X-axis: Right atrial pressure (independent variable) • Y-axis: Cardiac output (dependent variable) • Slope of curve: Defined by contractility, afterload, and heart rate

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Cardiology: Cardiac Function and Venous Return Curve Physiology

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Venous Return Curve: • X-axis: Right atrial pressure (dependent variable) • Y-axis: Cardiac output (independent variable) • Slope of curve: Defined by total peripheral resistance • X and Y intercept: Defined by venous compliance and total blood volume

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Cardiology: Cardiac Function and Venous Return Curve Physiology

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Intersection: • Steady state operating target for right atrial pressure and cardiac output Variables: • Slope of Cardiac Function Curve à Contractility, Heart rate, Afterload • Slope of Venous Return Curveà TPR • X-intercept of Venous Return Curve (Pm) à Total blood volume, Venous compliance

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Cardiology: Cardiac Function and Venous Return Curve Physiology

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Acute Hemorrhage: Disruption: ↓ blood volume • Cardiac Function Curve: No change • Venous Return Curve: X-intercept shifts left • Steady State: Shifted downward and to the left Intravenous Fluids: Disruption: ↑ blood volume • Cardiac Function Curve: No change • Venous Return Curve: X-intercept shifts right • Steady State: Shifted upward and to the right Chronic Systolic Heart Failure: Disruption: ↓ contractility, Chronic à Compensation • Cardiac Function Curve: ↓ slope • Venous Return Curve: Slope decreases, X-intercept shifts right • Steady State: Shifted downward and to the right Digoxin: Disruption: ↑ contractility • Cardiac Function Curve: ↑ slope • Venous Return Curve: Slope unchanged, X-intercept unchanged • Steady State: Shifted upward and to the left Phenylephrine: Disruption: ↑ TPR (!1-agonist) • Cardiac Function Curve: ↓ slope • Venous Return Curve: ↓ slope , X-intercept unchanged (usually) • Steady State: Shifted downward Hydralazine: Disruption: ↓ TPR • Cardiac Function Curve: ↑ slope • Venous Return Curve: ↑ slope , X-intercept unchanged (usually) • Steady State: Shifted upward

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Slope of Cardiac Function Curve à Contractility, Heart rate, Afterload Slope of Venous Return Curveà TPR X-intercept of Venous Return Curve (Pm) à Total blood volume, Venous compliance

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A 67-year-old male with a chronic smoking history presents to the emergency department by paramedics with hypotension refractory to intravenous fluids following an episode of syncope at home. His daughter reports he suddenly loss consciousness while watching television. Vitals are significant for a blood pressure of 88/28 mmHg, heart rate of 124/min, and respiratory rate of 18/min. Imaging reveals findings consistent with an aortocaval fistula. Surgery is emergently performed.

⚪ A. ⚪ B. ⚪ C. ⚪ D. ⚪ E.

Cardiac Output Venous Return

Which of the following new steady states are most representative of the acute pathophysiology observed in this patient prior to surgical intervention?

A. B. E. C. Right Atrial Pressure

(E.) Prior to aortocaval fistula D.

OUTLINE

Cardiology: Pressure Volume Loops

1.

Basic Principles

● A. Key Principles ● B. Phases 2. Determinants A. Preload ● B. Contractility ● ● C. Afterload 3. Valvular Disease ● A. Aortic Regurgitation ● B. Aortic Stenosis ● C. Mitral Regurgitation ● D. Mitral Stenosis 4. Advanced Pathophysiology ● A. Exercise ● B. Arteriovenous Fistula ● C. Systolic Heart Failure ● D. Diastolic Heart Failure

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Cardiology: Pressure Volume Loops

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Key Principles: • All valves are closed during isovolumetric phases (vertical lines) • Width of the pressure volume loop ~ Stroke Volume • Area of pressure volume loop ~ Ventricular Stroke Work • Ventricular compliance makes up the base of the loop Phases: • Isovolumetric contraction • Left ventricular ejection • Isovolumetric relaxation • Ventricular filling

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Cardiology: Pressure Volume Loops

Bootcamp.com https://commons.wikimedia.org/wiki/File:Cardiac_cycle_(pressure_volume_loop).svg

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Preload: • ↑ à EDV shifts right • ↓ à EDV shifts left

•

Contractility: • ↑ à ESV shifts left • ↓ à ESV shifts right

•

Afterload: • ↑ à ESV shifts right • ↑ à ↑ LVP isovolumetric contraction • ↓ à ESV shifts left • ↓ à ↓ LVP isovolumetric contraction

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Cardiology: Pressure Volume Loops

• • • •

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Hemorrhagic Shock: • ↓ Total blood volumeà ↓ Preload Intravenous Fluids: • ↑ Total blood volumeà ↑ Preload Nitroglycerin: • Venodilator (primary)à ↓ Preload • Vasodilator (secondary)à ↓ Afterload Sodium Nitroprusside: • Vasodilator (primary)à ↓ Afterload, ↓ TPR (↓ DBP) • Venodilator (primary) à ↓ Preload

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Cardiology: Pressure Volume Loops

•

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Digoxin, Dobutamine: • Inotropic agentà ↑ Contractility • Slight increases in ventricular afterload are possible

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https://en.wikipedia.org/wiki/Press ure%E2%80%93volume_loop_ana lysis_in_cardiology#/media/File:En d_Systolic_Pressure_Volume_Rel ationship.jpg

Cardiology: Pressure Volume Loops

• •

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Phenylephrine: • !1-agonist à ↑ Afterload, ↑ TPR (↑ DBP) Hydralazine: • Vasodilatorà ↓ Afterload, ↓ TPR (↓ DBP)

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Cardiology: Pressure Volume Loops

• • •

•

Aortic Regurgitation: • Retrograde flow of oxygenated blood into LV à ↑ Preload • Loss of isovolumetric phases Aortic Stenosis: • Stenosis distal to left ventricle à ↑ Afterload • Chronic: ↓ Ventricular compliance (Diastolic heart failure) Mitral Regurgitation: • Retrograde flow of oxygenated bloodAfraTafreeh.com into LA à ↑ Preload • Loss of isovolumetric phases Mitral Stenosis: • Stenosis proximal to left ventricle à ↓ Preload https://en.wikipedia.org/wiki/Pressure%E2%80%93volume_loop_analysis_in_cardiology#/media/ File:Mitral_stenosis.jpg

https://en.wikipedia.org/wiki/Pressure%E2%80%93volume_loop_analysis_in_cardiology#/media/ File:Mitral_regurgitation.jpg https://en.wikipedia.org/wiki/Pressure%E2%80%93volume_loop_analysis_in_cardiology#/media/ File:Aortic_regurgitation.jpg https://en.wikipedia.org/wiki/Pressure%E2%80%93volume_loop_analysis_in_cardiology#/media/ File:Aortic_stenosis.jpg

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Cardiology: Pressure Volume Loops

•

•

• •

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Exercise: • Venoconstriction, muscle and respiratory pumps à ↑ Preload • Sympathetic stimulation to heart à ↑ Contractility • Muscle vasodilation < ventricular afterload à ↑ Afterload (↓ DBP) Arteriovenous Fistula: • Low resistance fistulaà ↓ Afterload • High flow of blood through fistula à ↑ Venous return, ↑ Preload • If fistula is large à hypotension à ↑ Contractility, heart rate à High-output cardiac failure Systolic Heart Failure • Principal determinant: ↓ Contractility • Chronic à ↓↓↓ Contractility, ↑ Preload, ↓ Afterload Diastolic Heart Failure • Principal determinant: ↓ Ventricular compliance • Chronic: ↓ Preload, variable changes in contractility and afterload • Key point: Decrease in stroke volume and compliance

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A 57-year-old male with presents to an urgent care clinic with a numbness of his right foot and shortness of breath. He states that he had three fall episodes over the past month because “he can’t feel the floor”. He denies any dizziness and reports that he has not been seen by a physician in over twenty years. Physical examination reveals a left internuclear ophthalmoplegia. The pupils accommodate but are not reactive to direct or indirect light stimulation. Locally destructive ulcerative lesions are present diffusely throughout the face and upper back. Cardiovascular examination demonstrates a high-pitched diastolic murmur most prominent at the left fourth intercostal space along the left sternal border. Pulses are notable for a rapid upstroke and downstroke. Reflexes are 1+ at L4 and C5 bilaterally. Sensory ataxia is also present.

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A biopsy of the skin lesions is taken revealing a monocytic infiltrate. The patient is referred for a lumbar puncture. Which of the following best demonstrates the time along the left ventricular pressure-volume loop that this patient’s heart murmur will be most prominent?

⚪ A. Distance between A to B ⚪ B. Distance between B to C ⚪ C. Distance between C to D ⚪ D. Distance between D to A ⚪ E. Point D

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https://en.wikipedia.org/wiki/Pressure%E2%80%93volume_diagram

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Cardiology: Vasodilation and Vasoconstriction

1.

Endothelial Regulated Vasodilation

● A. Mechanism of Action 2. Excitation-Contraction Coupling ● A. Cardiac Myocyte ● B. Vascular Smooth Muscle ● C. Skeletal Muscle 3. G-Protein Coupled Receptor Vasoconstriction Pathway ● A. Gq Pathway 4. Pharmacologic Targets ● A. !1 agonists ● B. Nonhydropyridine Calcium Channel Blockers ● C. Dihydropyridine Calcium Channel Blockers ● D. Phosphodiesterase-3 Inhibitors ● E. Additional Vasodilatory Drugs

Cardiology: Vasodilation and Vasoconstriction

•

•

Endothelial Cell: • Acetylcholine, bradykinin, and shear stress forces à ↑ cytosolic [Ca2+] • Nitric oxide Synthase stimulated by ↑ [Ca2+] • L-Arginine + O2 à Nitric oxide + Citrulline • Nitric oxide diffuses freely among cells Vascular Smooth Muscle: • Nitric oxide causes increased conversion of GTP à cGMP • cGMP à activation of PKG à ↓ cytosolic [Ca2+] • Relaxation of vascular smooth muscle AfraTafreeh.com

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Cardiology: Vasodilation and Vasoconstriction

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https://upload.wikimedia.org/wikipedia/commons/1/10/Cardiac_calcium_cycling_and_excitation-contraction_coupling.png

•

Cardiac Myocytes • Depolarization of cell membrane by action potential • L-type calcium channel: influx of calcium ions from extracellular • Calcium-induced calcium release: incoming calcium ions bind to ryanodine receptor • Ryanodine receptor: influx of calcium ions from SR • Calcium ions bind to troponin-C • Conformational change allows actin to interact with myosin head • SERCA: Sequesters intracellular calcium into SR via ATP à relaxation

•

Smooth Muscle: • Depolarization of cell membrane by action potential • L-type calcium channel: influx of calcium ions from extracellular • Calcium induced calcium release • Calcium ions bind to calmodulin • Conformation change in myosin light chain kinase (MLCK) • Phosphorylates myosin light chain (MLC) à contraction • Myosin light chain phosphatase dephosphorylates MLC à relaxation

•

Skeletal Muscle (Major Differences from Cardiac Myocytes): • Pathway stimulated by acetylcholine (not automaticity) • Mechanical coupling of LTCC with RyR

Cardiology: Vasodilation and Vasoconstriction

•

Gq-GPCR Mechanism: • Present on arterioles (↑ afterload) and veins (↑ preload) • Gq protein à ↑ Phospholipase C (PLC) • PIP2 à ↑ inositol triphosphate (IP3) + Diacylglycerol (DAG) • IP3 à ↑ cytosolic [Ca2+] (from ER) • DAG à Protein Kinase C (PKC) à ↑ cytosolic [Ca2+] (from extracellular space)

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Cardiology: Vasodilation and Vasoconstriction

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https://upload.wikimedia.org/wikipedia/commons/1/10/Cardiac_calcium_cycling_and_excitation-contraction_coupling.png

•

•

•

•

•

!1-agonists • Activation of Gq-GPCR pathway • Primary effect: Vasoconstriction • Drugs: Phenylephrine (selective), norepinephrine (nonselective) Nondihydropyridine Calcium Channel Blockers: • Inhibition of L-type calcium channels • Greater effect on calcium-induced calcium release • Primary effect: ↓ Contractility, bradycardia, AV block • Drugs: Verapamil, diltiazem Dihydropyridine Calcium Channel Blockers: • Inhibition of L-type calcium channels • Greater effect on calcium-induced calcium release • Primary effect: Vasodilation • Drugs: Nifedipine, nicardipine, felodipine, amlodipine (arterial > venous) Phosphodiesterase-3 (PDE-3) Inhibitor: • PDE-3 à Inhibition of cAMP degradation (myocytes) and ↑ SR calcium uptake (vascular) • Primary effect: ↑ Contractility, vasodilation • Drugs: Milrinone, Cilostazol, Dipyridamole Additional Vasodilatory Drugs: • Nitric oxide (venous > arterial) • Hydralazine, minoxidil (arterial > venous) • Nitroprusside (arterial = venous) • Sildenafil (PDE-5 inhibitor) à (pulmonary and corpus cavernosum)

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A 77-year-old male is brought to the emergency department from his living facility with lethargy. Vital signs reveal a blood pressure of 58/20 mmHg, heart rate 122 beats/min, respiratory rate 20 breaths/min, oxygen saturation 91% on room air, and a temperature of 103.3F (39.6C). Initial labs reveal a lactate of 9.0 and white blood cell count of 18,000/mm3. He is aggressively fluid resuscitated and started on slow intravenous phenylephrine injection for blood pressure support. Which of the following cellular changes are most likely to occur due to the direct effects of the medication given?

AfraTafreeh.com ⚪ A. Increased inhibition of adenylyl cyclase ⚪ B. Decreased intracellular concentrations of L-arginine ⚪ C. Decreased cyclic AMP degradation ⚪ D. Increased myosin light chain phosphatase activity ⚪ E. Decreased degradation of adenosine ⚪ F. Increased intracellular concentrations of inositol triphosphate

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Cardiology: Pressure and Flow Physiology

1. Vessel Compliance ● A. Key Principles 2. Blood Flow ● A. Poiseuille Equation ● B. Resistance 3. Sensory Receptors of the Vasculature ● A. Carotid Sinus and Aortic Arch Baroceptors ● B. Carotid Sinus Massage ● C. Carotid Sinus Hypersensitivity D. Carotid and Aortic Body Chemoreceptors ●

Cardiology: Pressure and Flow Physiology

•

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Vessel Compliance: • Compliance = ∆Volume / ∆Pressure • Elastance = ∆Pressure / ∆Volume • ↑ Compliance à Veins • ↓ Compliance à Arterioles

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Cardiology: Pressure and Flow Physiology

•

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Poiseuille Equation: !" #!$ 4 • Flow (Q) = rπ 8%&

• • • • • •

Q = Flow P = Pressure at point in blood vessel ! = viscosity of blood within blood vessel l = length of blood vessel r = radius of blood vessel Capillaries have greatest total cross-sectional area à lowest blood velocity

• • • • • •

Resistance: %& R∝ ! ' R = Resistance Arterioles are the primary regulator of total peripheral resistance Series: Total Resistance = RT = R1 + R2 + …Rn Parallel: Total Resistance = 1/%T = 1/%1 + 1/%2 + … 1/%n

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Cardiology: Pressure and Flow Physiology

• •

•

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Carotid Sinus and Aortic Arch Baroceptors: • ↑ stretch (↑ BP) à ↑ afferent ↑ efferent PNS firing à ↑ parasympathetic response à vasodilation, ↓ HR, ↓ contractility • ↓ stretch (↓ BP) à ↓ afferent ↓ efferent PNS firing à ↓ parasympathetic response à vasoconstriction, ↑ HR, ↑ contractility Carotid Sinus Massage: • ↑ afferent ↑ efferent PNS firing à ↑ parasympathetic response à vasodilation, ↓ HR, ↓ contractility • Stable narrow complex tachycardia à Vagal maneuver Carotid Sinus Hypersensitivity: • Develops severe hypotension and/or bradycardia after carotid sinus stimulation • “Tight shirt collar” • Presyncopal/syncopal event Carotid and Aortic Body Chemoreceptors: • Effective at responding to chronic hypoxia (as opposed to central chemoreceptors) • ↓ O2 (↑ CO2, ↓ pH) à ↑ sympathetic response à ↑ respiratory rate

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A 78-year-old female with a past medical history of dyslipidemia, hypertension, and type 2 diabetes mellitus is evaluated at an acute rehabilitation facility for dizziness during therapy. She denies any shortness of breath, vision changes, or chest pain. The patient has a history of C3-C5 laminectomy for severe spinal stenosis. Vital signs are shown below. Auscultation of the heart reveals a regular rate and rhythm with no murmurs or abnormal heart sounds. The lungs are clear to auscultation. Which of the following undiagnosed conditions best describes a possible cause of this patient’s presentation? Temperature: 97.8F (36.6C) Blood pressure when lying supine: 144/88 mmHg Heart rate when lying supine: 102/min Respiratory rate when lying supine: 12/min Blood pressure when standing: 110/56 Heart rate when standing: 112/min Respiratory rate when standing: 14/min

⚪ A. Carotid sinus hypersensitivity ⚪ B. Autonomic neuropathy ⚪ C. Neurogenic shock ⚪ D. Constrictive pericarditis ⚪ E. Hypertrophic cardiomyopathy

OUTLINE

Cardiology: Cardiac Cycle

1. Auscultation

5.

Classic Disorders

● A. Aortic Area ● B. Pulmonic Area ● C. Mitral Area ● D. Tricuspid Area ● E. Erb’s Point 2. Heart Sounds ● A. S1 B. S2 ● ● C. Physiologic Splitting of S2 ● D. Pathologic Splitting of S2 ● E. S3 ● F. S4 3. Cardiac Cycle ● A. Isovolumetric Contraction B. Ejection ● ● C. Isovolumetric Relaxation D. Ventricular Filling ● E. Atrial Systole ● 4. Jugular Venous Waveform ● A. A-wave ● B. C-wave ● C. X-descent ● D. V-wave ● E. Y-descent

● ● ● ● ● ● ● ●

A. Aortic Stenosis B. Aortic Regurgitation C. Mitral Stenosis D. Mitral Regurgitation E. Constrictive Pericarditis F. Cardiac Tamponade G. Atrial Fibrillation H. AV-dissociation

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Cardiology: Cardiac Cycle

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https://en.wikipedia.org/wiki/Heart_sounds#/media/File:Gray1216_modern_locations.svg

• • • • •

Aortic Area: • 2nd R parasternal ICS Pulmonic Area: • 2nd L parasternal ICS Tricuspid Area: • 4th L parasternal ICS Mitral Area: • 5th L mid-clavicular line ICS Erb’s Point • 3rd L parasternal ICS

Cardiology: Cardiac Cycle

•

• •

•

S1: • •

Produced by: Closure of tricuspid and mitral valves Best heard: Cardiac apex Accentuation: Left lateral decubitus position in expiration

S2: • Produced by: Closure of the pulmonary (P2) and aortic valve (A2) • Best heard: P2 à 2nd L parasternal ICS A2 à 2nd R parasternal ICS Physiologic S2 Splitting: • Narrowing à Expiration AfraTafreeh.com • Widening à Inspiration Pathologic S2 Splitting: • Wide Fixed à Atrial septal defect • Wide à Pulmonary stenosis, Right bundle branch block • Paradoxical à Severe aortic stenosis, Left bundle branch block

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Cardiology: Cardiac Cycle

•

S3: • • • • •

•

S4: • • • • •

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Produced by: Rapid passive ventricular filling (↑ left ventricular volumes) Best heard: Cardiac apex (bell) Accentuation: Left lateral decubitus position in expiration Timing: Early diastole, after S2 (gallop) Physiologic: Young and fit, pregnancy Pathologic: Heart failure (systolic), mitral regurgitation, aortic regurgitation Produced by: Atrial kick (↑ left ventricular pressures) Best heard: Cardiac apex (bell) Accentuation: Left lateral decubitus position in expiration Timing: Late diastole, before S1 Physiologic: Elderly Pathologic: Heart failure (diastolic), chronic hypertension, aortic stenosis

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Cardiology: Cardiac Cycle

Bootcamp.com https://commons.wikimedia.org/wiki/File:Wiggers_Diagram.svg

•

•

Isovolumetric Contraction: • Begins after closing of mitral valve (S1) • Highest oxygen consumption • QRS complex on ECG à ventricular depolarization Ejection: • Begins after opening of the aortic valve • Rapid Ejection: Rising LVP, ↓↓ LV volume • Reduced Ejection: Decreasing LVP

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Cardiology: Cardiac Cycle

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Bootcamp.com https://commons.wikimedia.org/wiki/File:Wiggers_Diagram.svg

•

•

•

Isovolumetric Relaxation: • Begins after closing of aortic valve (S2) • Dicrotic notch • Coronary blood flow peaks Ventricular Filling: • Begins after opening of the mitral valve • Rapid Fillin • S3: Rapid filling into volume overload LV • Reduced Filling Atrial Systole: • At conclusion of diastole • S4: Atrial kick into “stiff” ventricle

Cardiology: Cardiac Cycle

Bootcamp.com https://commons.wikimedia.org/wiki/File:Wiggers_diagram_with_jugular_venous_waveform.png

• •

• • •

•

A-wave: • Atrial systole (P wave) C-wave: • Ventricular contraction • Tricuspid valve protrudes into atrium X-descent: • Atrial relaxation V-wave: • Atrial filling à tricuspid valve “back-pressure” AfraTafreeh.com Y-descent: • Ventricular filling

Classic Disorders: • Atrial fibrillation: Absent A-waves (absent P-waves on ECG) • Tricuspid (or Mitral) regurgitation: ↑ V-wave > A-wave • Tamponade: Blunting of Y-descent • Constrictive pericarditis: Increased Y-descent • Atrial contraction against closed tricuspid: “Cannon” A-waves

Cardiology: Cardiac Cycle

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https://commons.wikimedia.org/wiki/File:Wiggers_diagram_with_jugular_venous_waveform.png

• •

• •

Aortic Stenosis: • LVP >> Aortic pressure Aortic Regurgitation: • ↑ Aortic pressure during systole • ↓ Aortic pressure at the end of diastole • ↑ Pulse pressure (SBP - DBP) • Loss of dicrotic notch Mitral Stenosis: • LAP > LVP during diastole Mitral Regurgitation: • Tall V-wave (similar to tricuspid regurgitation)

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https://upload.wikimedia.org/wikipedia/commons/7/75/Pulmonary_oedema.jpg

A 56-year-old male with a past medical history of alcohol use and withdrawal seizures is brought to the emergency department from a homeless shelter with acute onset confusion, ataxia, and agitation. He is unable to recall the time of his last drink. Blood pressure is 168/68, heart rate is 126/min, respiratory rate is 16/min. On physical examination he appears to have diffuse muscular atrophy and peripheral edema in the distal lower extremities. The patient also appears tremulous and has visible nystagmus on testing of the extraocular muscles. An electrocardiogram is performed showing sinus tachycardia with no evidence of ST-segment elevation or depression. Chest radiography is shown below. Which of the following additional examination findings would be most expected in this patient? ⚪ A. Wide-fixed splitting of S1 heart sounds ⚪ B. Wide-fixed splitting of S2 heart sounds ⚪ C. Prominent S3 heart sound ⚪ D. Prominent S4 heart sound ⚪ E. Paradoxical splitting of S2 heart sounds

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Cardiology: ReninAngiotensinAldosterone System

1.

Regulation

● A. Renin ● B. Angiotensin Converting Enzyme ● C. Angiotensin II ● D. Natriuretic Peptides 2. Direct Pharmacologic Targets ● A. Angiotensin Converting Enzyme Inhibitors ● B. Angiotensin Receptor Blockers ● C. Direct Renin Inhibitors ● D. Neprilysin Inhibitors ● E. β1-antagonism

Cardiology: RAAS

Bootcamp.com https://en.wikipedia.org/wiki/Juxtaglomerular_apparatus#/media/File:Renal_corpuscle-en.svg

•

•

Renin • Location: Juxtaglomerular apparatus • Stimulus: ↑↑ Renin: β1 stimulation, ↓ pressure in renal artery, ↓ Na to distal tubules (kidney) • Function: Converts Angiotensinogen to Angiotensin I Angiotensin Converting Enzyme (ACE) • Location: Lungs (primarily) • Function: Angiotensin I converted to Angiotensin II (ATII) by ACE

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Cardiology: RAAS

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Bootcamp.com https://commons.wikimedia.org/wiki/File:Renin-angiotensin-aldosterone_system.svg

•

Actions Angiotensin II: • ↑ Vasoconstriction (↑ TPR) • ↑ Norepinephrine release and availability • ↑ Na reabsorption, ↑ blood volume • Stimulates aldosterone release from zona glomerulosa • Stimulates vasopressin (ADH) release from posterior pituitary

Cardiology: RAAS

Bootcamp.com https://commons.wikimedia.org/wiki/File:Renin-angiotensin-aldosterone_system.svg

•

•

Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP) • Location: Myocardium • Stimulus: ↑ Atrial and ventricular pressures • Function: ↑ Vasodilation, ↑ Diuresis, inhibition of aldosterone and renin release • Attempts to compensate (temporarily) for ATII in heart failure Molecular Mechanism: • ↑ cGMP à stimulates vasodilation and diuresis

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Cardiology: RAAS

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Bootcamp.com https://commons.wikimedia.org/wiki/File:Renin-angiotensin-aldosterone_system.svg

•

• • • •

ACE Inhibitors (Lisinopril, Captopril, Enalapril, -pril) • Inhibition of ACE à ↑ angiotensin I and renin, ↓ angiotensin II • Use: Hypertension, Nephroprotective effects (Diabetes), Cardioprotective effects (Heart failure) • Adverse Effect: Dry cough, hyperkalemia, angioedema Angiotensin Receptor Blockers (ARBs) (Valsartan, Losartan, -sartan) • Receptor blockade of angiotensin II type 1 receptor • Use: Hypertension, Nephroprotective effects (Diabetes), Cardioprotective effects (Heart failure) Direct Renin Inhibitors (Aliskiren) • Inhibition of conversion of angiotensinogen to angiotensin I • Use: Hypertension (not first line) Neprilysin Inhibitors (Sacubitril) • Neprilysin inactivates ANP, BNP and AT-II • Use: Heart failure when combined with angiotensin-II receptor inhibitor Selective β1-blockers (Metoprolol, Nebivolol, Esmolol, Atenolol) • Antagonism of β1 receptors at juxtaglomerular apparatus • Use: Coronary artery disease, cardiac arrhythmias (and many more) • Adverse Effect: Bradycardia, bradyarrhythmia (AV nodal block)

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A 68-year-old female with a past medical history of osteoarthritis and hyperthyroidism presents to the emergency department with shortness of breath. She states that she has been having palpitations for the past two hours. She reports running out of her thyroid medication five weeks prior and has not yet refilled her prescription. She is later diagnosed with new onset atrial fibrillation with rapid ventricular response. She is initiated on metoprolol for rate control. Which of the following primary changes in chemical mediators will likely occur due to the initiation of this medication?

⚪ A. ⚪ B. ⚪ C. ⚪ D. ⚪ E.

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Renin

Angiotensin I

Angiotensin II

Aldosterone

↑ ↑ ↑ ↑ ↓

↑ ↑ ↑ ↓ ↓

↑ ↑ ↓ ↓ ↓

↑ ↓ ↓ ↓ ↓

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Cardiology: Exercise Physiology

1. ● ● ● ● ● ● ● ● ●

A. B. C. D.

2. ● ●

A. B.

. ● ●

A. B.

Cardiology: Exercise Physiology

•

• • • • • • •

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↑ Preload • Venoconstriction à ↑ Venous return à ↑ LVEDV • Vasoconstriction of splanchnic vessels • Vasodilation at skeletal muscle à ↓ SVR (↓ DBP) à ↓ Afterload ↑ Contractility ↓ Afterload • Can be variable depending on dynamic vs static, muscle groups recruited, intensity, ect. ↑ Heart Rate • ↑ Sympathetic tone (↓ Vagal tone) ↓ Coronary Perfusion • ↓ Time spent in diastole at high heart rates ↑ Minute Ventilation • ↑ O2 demand à ↑ RR, ↑TV à ↑ O2 consumption and CO2 production ↑ Temperature ↓ Arterial pH • ↑ Lactic acidosis

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Cardiology: Exercise Physiology

• •

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Fick Principle à Cardiac Output = Rate of O2 consumption / Arteriovenous O2 difference • VO2 = Rate of oxygen consumption Oxygen Extraction Efficiency: • PaO2 relatively normal • PaCO2 relatively normal • Venous O2 decreased • Venous CO2 increased

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Cardiology: Exercise

•

•

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General Rules: • Max HR = 220 - Age • Early exercise à HR and SV responsible for ↑ CO • Intense exercise à HR primarily responsible for ↑ CO Athletic Cardiovascular Physiology: • Max HR not affected by athletic ability • Stroke volume primarily responsible for ↑↑ CO • ↑ VO2 maximum • ↑ RBC mass and plasma volume à ↑ O2 carrying capacity • ↑ Efficiency of skeletal muscle oxygen extraction • ↑ Vascularization of skeletal muscle • ↓ resting heart rate

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Temperature: 97.2F (36.2C) Blood pressure: 110/62 mmHg Heart rate: 52/min Respiratory rate: 10/min Oxygen saturation: 100% on room air Which of the following is most consistent with the hemoglobin-oxygen dissociation curve of the patient during the upcoming cycling event, assuming the blue curve (A.) is consistent with her baseline at rest? ⚪A ⚪ B. ⚪ C. ⚪ D. ⚪ E.

Hemoglobin O2 Saturation (%)

A 26-year-old female professional cyclist is training for a 143km bicycle-road race. She is seen by her primary care physician one week prior to the event for a check-up. Vital signs are shown below. Her physical examination is unremarkable.

Arterial Partial Pressure of O2 (mmHg)

OUTLINE

Cardiology: Cardiac Conductive Physiology

1. ● ● ● ● ●

A. B. C. D. E.

2. ● ●

A. B.

3. ● A. AfraTafreeh.com ● B. ● . ● ● ● ●

A. B.

Cardiology: Cardiac Conductive Physiology

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https://en.wikipedia.org/wiki/Purkinje_fibers#/media/File:ConductionsystemoftheheartwithouttheHeart-en.svg

Cardiac Conduction Velocity •

•

•

•

Sinoatrial (SA) Node • Site of electrical impulse generation • Pacer rate of 60-100 per minute • Supplied by RCA Atrioventricular (AV) Node • Delays conduction from SA node • Pacer rate of 45-55 per minute • Supplied by PDA (usually RCA) Bundle of His • Prevents retrograde electrical conduction • Right Bundle à Right ventricle • Left Bundle à Left ventricle (anterior and posterior) Purkinje Fibers • Transmits conduction across ventricles

Purkinje > Atrial myocytes > Ventricular myocytes > AV node

Cardiology: Cardiac Conductive Physiology

Bootcamp.com https://commons.wikimedia.org/wiki/File:2020_SA_Node_Tracing.jpg

•

Pacemaker Cells • Exhibit automaticity (spontaneous depolarization) • Absence of Phase 1 and 2 • Phase 4 is a slow depolarization phase

•

Phase 4: Pacemaker Potential • Begins with: ↑ Permeability of inward Na+ (If) current à Slow, spontaneous depolarization • Then: ↑ Permeability T-type and L-type Ca2+ current à Further depolarization Phase 0: Action Potential Depolarization • Begins when threshold is reached • Na+ current and T-type calcium current decreases • Increased L-type Ca2+ current à Action potential depolarization Phase 3: Action Potential Repolarization • Outward K+ current à Hyperpolarization • Inward L-type Ca2+ current decreases (inactivation)

•

•

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Cardiology: Cardiac Conductive Physiology

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https://en.wikipedia.org/wiki/Ventricular_action_potential#/media/File:Action_potential_ventr_myocyte.gif

•

Non-Pacemaker Cells • Do not exhibit automaticity • Phases 0-4 are present • Phase 4 is a resting potential phase (approximates equilibrium potential of potassium)

•

Phase 4: Resting Membrane Potential • ↑ Permeability of outward K+ current • Fast Na+ channels and L-type Ca2+ channels are closed Phase 0: Action Potential Depolarization • Begins with depolarization from action potential at adjacent cell • ↑ Permeability of inward fast Na+ current • ↓ Permeability of outward K+ current Phase 1: Early Repolarization • Transient ↑ permeability of outward K+ current • Rapid closure of fast Na+ channels (inactivation) Phase 2: Plateau Phase • L-type Ca2+ channels are open and balance K+ efflux Phase 3: Late Repolarization • Various K+ channels open à ↑↑ permeability outward K+ current • Inactivation of L-type Ca2+ channels

•

•

• •

Cardiology: Cardiac Conductive Physiology

• • • •

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https://en.wikipedia.org/wiki/Long_QT_syndrome#/media/File:Long_QT_syndrome_type_1.jpg https://www.wikidata.org/wiki/Q1625433#/media/File:Tosadesdepointes.jpg

Sympathetic Stimulation Effects on Pacemaker Potentials • β1 stimulation à ↑ cAMP à ↑ permeability of inward calcium current à ↑ HR Parasympathetic Stimulation Effects on Pacemaker Potentials • M2 stimulation à ↓ cAMP à ↓ permeability of inward calcium current à ↓ HR Sodium Channelopathy: • Impairment of inward fast Na+ current (Phase 0) • Brugada Syndrome: AD, ECG: ST-elevation in V1-V3, pseudo-RBBB QT Interval Prolongation • Delayed ventricular repolarization • Impairment of voltage-gated potassium channels à delayed rectifier potassium current • May lead to torsade de pointes (“twisting of the peaks”), ventricular tachycardia à sudden cardiac death • Romano-Ward Syndrome: AD, no associated sensorineural hearing loss • Jervell and Lange-Nielsen Syndrome: AR, associated congenital bilateral sensorineural hearing loss • Drug Induced: *see table below*

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Class

Classic Drug

Other Drugs/Effects

A

Antiarrhythmics

Quinidine

Disopyramide, procainamide, sotalol, dofetilide

B

Antibiotics

Macrolides

Fluoroquinolones

C

Antipsychotics

Haloperidol

Ziprasidone

D

Antidepressants

Tricyclic antidepressants

Methadone

E

Antiemetics/Electrolytes

Ondansetron

Hypocalcemia, hypokalemia, hypomagnesemia

F

Antifungals

Azoles

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A 14-year-old male with a past medical history of mild intermittent asthma presents to the emergency department with a productive cough and mild shortness of breath that started before going to school this morning. His mother reports that he has been nauseous this morning and hasn’t eaten his breakfast. She also states that he has a family history of “bad luck with the heart” on his father’s side. His father is deceased from unknown cause of sudden cardiac death at age 38. The patient is up to date with vaccinations. Vitals are stable and he is saturating 99% on room air. Mild end-expiratory wheezing is auscultated. Laboratory workup is unrevealing. The patient is given a single dose of azithromycin and ondansetron. He is monitored in the emergency room. The patient’s respiratory symptoms improve, and he is prescribed a short-acting inhaled beta-agonist on discharge. Four hours later, the patient returns to the emergency room with his mother for acute worsening of shortness of breath. Electrocardiogram findings from lead II are shown below. Which of the following most likely explains the cause of this patient’s return to the emergency department?

⚪ A. Decreased inward calcium current in pacemaker cells ⚪ B. Decreased inward calcium current in cardiomyocytes ⚪ C. Decreased inward sodium current in cardiomyocytes ⚪ D. Decreased outward potassium current in cardiomyocytes ⚪ E. Increased outward potassium current in pacemaker cells

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OUTLINE

Cardiology: Antiarrhythmics

1. ● ● ● ●

A. B. C. D.

2. ● ● ● ●

A. B.

AfraTafreeh.com . ● ● ●

A.

● . ● ● ●

A.

Cardiology: Antiarrhythmics

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Bootcamp.com https://en.wikipedia.org/wiki/Antiarrhythmic_agent#/media/File:Cardiac_action_potential.png

Overview • • • •

Class I • Three subclasses: Class IA, IB, IC • Blockade of fast Na+ channels Class II • β-blockers • Delayed atrial ➔ ventricular depolarization Class III • Blockade of potassium channels Class IV • Calcium channel blockers • Delayed atrial ➔ ventricular depolarization

Cardiology: Antiarrhythmics

https://commons.wikimedia.org/wiki/File:Action_potential_class_Ic.svg

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https://commons.wikimedia.org/wiki/File:Action_potential_class_Ia.svg https://commons.wikimedia.org/wiki/File:Action_potential_Class_Ib.svg

•

•

Class IA • Quinidine, Procainamide, Disopyramide • Mechanism: Moderate blockade of fast Na+ channels (Non-pacemaker) • ↑ Action potential duration • Widening of QRS, QT prolongation • Quinidine à Cinchonism • Drug-Induced Lupus à Procainamide Class IB • Lidocaine, Mexiletine, Phenytoin • Mechanism: Weak blockade of fast Na+ channels (Non-pacemaker) • ↓ Action potential duration • QRS prolongation, shortened QT interval • ↑↑ Efficacy on ischemic Purkinje and ventricular myocardial cells Class IC • Flecainide, Propafenone • Mechanism: Strong blockade of fast Na+ channels

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•

• •

•

• • • •

QRS prolongation, no significant change in QT (Exceptions exist) Flecainide à ↑ Action potential duration Contraindicated in ischemic heart disease (Proarrhythmic)

Cardiology: Antiarrhythmics

•

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Class II • Metoprolol, Esmolol, Propranolol, Atenolol, Carvedilol • Mechanism: Inhibition of cAMP à ↓ intracellular Ca2+ • Prolonged Phase 4 (Pacemaker) • PR prolongation

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Cardiology: Antiarrhythmics

•

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Class III • Sotalol, Ibutilide, Dofetilide • Mechanism: Inhibition of K+ channels (delayed rectifier potassium current) • ↑ Action potential duration • QT prolongation à torsades de pointes • Sotalol prolongs PR interval; Ibutilide and Dofetilide do not

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Cardiology: Antiarrhythmics

•

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Class IV • Verapamil, Diltiazem • Mechanism: Inhibition of L-type Ca2+ channels (Pacemaker) • Prolonged Phase 0 and Phase 4 (Pacemaker) • PR prolongation

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Cardiology: Antiarrhythmics

•

• •

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Adenosine • Mechanism: Inhibition of L-type Ca2+ channels, ↑ K+ conductance • Prolonged Phase 4 (Pacemaker) • Classic use: Paroxysmal supraventricular tachycardia • Adverse effects: Sense of impending doom, flushing, chest pain Digoxin • Mechanism: Inhibition of Na+/K+ ATPase à ↑ intracellular Ca2+ • Adverse effects: Blurry, yellow discoloration to vision Magnesium • Mechanism: ↓ intracellular Ca2+ • Classic use: Torsades, digoxin toxicity Ivabradine • Mechanism: Inhibition of Na+ slow (funny) channels • Prolonged Phase 4 (Pacemaker) • Adverse effects: Visual luminous phenomenon (↑ visual brightness)

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A 38-year-old male with a past medical history of hypertension, mild intermittent asthma, and a recent diagnosis of pre-excitation cardiac conduction abnormalities, presents to his primary care physician for a fixed erythematous rash over the malar eminences with sparing of the nasolabial folds. He reports that the rash started after a long afternoon at the beach. He denies any pruritis or drainage from the lesion. He also reports feeling a dull, soreness in the deltoid region bilaterally. On physical exam multiple painless ulcers are noted along the oral mucosa. After a thorough review of the patient’s medications, a laboratory workup is performed and shown below.

Which of the following changes to the electrical conductivity is most likely occurring in ventricular cardiomyocytes as a result of iatrogenic causes in this patient?

Leukocyte count: 10,800/mm3 Hemoglobin: 13.7 g/dL Platelet count: 165,000/mm3 Sodium: 136 mEq/L Potassium: 4.4 mEq/L Chloride: 102 mEq/L Creatinine: 1.6 mg/dL Antinuclear (ANA) antibody: Positive for elevation in ANA titer Anti-double-stranded DNA antibody: Negative Antihistone antibody: Positive Anti-smith antibody: Negative Anti-Ro antibody: Negative

⚪ A. Increased potassium conductance ⚪ B. Decreased action potential duration ⚪ C. Increased action potential duration ⚪ D. Increased vagal nerve output to the atrioventricular node ⚪ E. Inhibition of L-type calcium channel conductance

OUTLINE

Cardiology: Atrial Arrhythmias

1. Atrial Fibrillation ● A. Pathophysiology ● B. Presentation ● C. Precipitating Factors ● D. Complications ● E. Rate Control ● F. Rhythm Control ● G. Catheter Ablation ● H. Anticoagulation ● I. Hemodynamics in Heart Failure ● J. Jugular Venous Pressure Tracing ● K. ECG Findings 2. Atrial Flutter ● A. Pathophysiology ● B. Presentation ● C. Precipitating Factors ● D. Management ● E. ECG Findings 3. Sick Sinus Syndrome ● A. Pathophysiology ● B. Presentation ● C. Association ● D. Management

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Cardiology: Atrial Arrhythmias

AfraTafreeh.com https://commons.wikimedia.org/wiki/File:Afib_ecg.jpg https://commons.wikimedia.org/wiki/File:Heart_conduct_sinus.gif https://commons.wikimedia.org/wiki/File:Heart_conduct_atrialfib.gif

• •

•

•

Pathophysiology: • Automatic foci in vicinity of pulmonary veins à structural fibrotic remodeling of atria à ↑ risk of occurrence • Rapid uncoordinated atrial contractions à AV node intermittently refractory à Rapid ventricular response Presentation: • Irregularly irregular rhythm, absence of P waves • Palpitations • Tachycardia • Shortness of breath, dizziness, palpitations Precipitating Factors: • Cardiovascular disease (Coronary artery disease, hypertension, heart failure) • Hyperthyroidism • Mitral stenosis • ↑ Sympathetic tone (cocaine, amphetamines, EtOH) Complications: • Embolic phenomena à left atrial appendage • Pulmonary edema • Ventricular tachycardia

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Cardiology: Atrial Arrhythmias

Bootcamp.com https://commons.wikimedia.org/wiki/File:Diagram_of_the_human_heart_(cropped).svg

• •

•

Rate Control: • β-blockers and CCBs: Preferred first-line • Digoxin: Second-line, useful in systolic dysfunction Rhythm Control: • Class IC Antiarrhythmics (Flecainide, propafenone) • Class III Antiarrhythmics (Ibutilide, sotalol) • Amiodarone Catheter Ablation: • Symptomatic paroxysmal atrial fibrillation à ablation at pulmonary vein ostia (left atrium) • Persistent atrial fibrillation with RVR à ablation can be at other sites like AV node (right atrium) • Amiodarone Anticoagulation Hemodynamics in Heart Failure • Left atrial dilatation • ↓ LV Preload à ↓ CO • ↑ PCWP • Pulmonary edema Jugular Venous Pressure Tracing • Loss of a waves

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• •

•

Cardiology: Atrial Arrhythmias

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Bootcamp.com https://commons.wikimedia.org/wiki/File:ECG_Atrial_Fibrillation.jpg

Absence of P waves Irregularly irregular (varying R-R intervals) Narrow QRS complexes

Cardiology: Atrial Arrhythmias

Bootcamp.com https://commons.wikimedia.org/wiki/File:Diagram_of_the_human_heart_(cropped).svg

• •

• •

Pathophysiology: • Re-entry circuit in right atrium (most common) Presentation: • Sawtooth appearance of P waves • Generally, regular rhythm (exceptions exist) • 2:1 conduction is most common • Tachycardia is common • Shortness of breath, dizziness, palpitations Precipitating Factors: • Similar to atrial fibrillation Management: • Rhythm control, rate control • Catheter ablation of re-entrant circuit (right atrium)

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Cardiology: Atrial Arrhythmias

AfraTafreeh.com https://commons.wikimedia.org/wiki/File:Brady-tachy_syndrome_AV-junctional_rhythm.png

• •

• •

Pathophysiology: • Fibrosis and degeneration of the SA node (usually age-related) • Iatrogenic (β-blockers, CCBs, Digoxin) Presentation: • Bradycardia, delayed P waves, dropped P waves • Junctional escape beats • Syncope, fatigue, shortness of breath • HR doesn’t increase as expected with exercise • Tachycardia-Bradycardia Syndrome Association: • Elderly Management: • Iatrogenic: Stop offending medications as necessary • Asymptomatic: Conservative • Acute (Unstable) Symptomatic: Atropine à Temporary cardiac pacing • Long Term (Stable) Symptomatic: Permeant Pacemaker placement, selective β-blockers

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A 46-year-old male with a past medical history of cocaine and alcohol use presents to the emergency room for palpitations. He states that he went out on a “binge” prior to arrival. His last drink was reported to have been five minutes prior to walking into the emergency department. An ECG strip is shown below. Which of the following is most likely directly related to the heart rate observed in this patient?

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⚪ A. Accessory pathway bypassing the atrioventricular node ⚪ B. Pacing initiation triggered at the atrioventricular node ⚪ C. Complete conduction through the atrioventricular node ⚪ D. Intermittent conduction through the atrioventricular node ⚪ E. Negligible conduction through the atrioventricular node

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AfraTafreeh.com OUTLINE 1.

Cardiology: Ventricular Arrhythmias and Pre-Excitation Syndromes

Supraventricular Tachycardia

● A. Pathophysiology ● B. Presentation ● C. ECG Findings ● D. Management 2. Wolff-Parkinson-White Syndrome ● A. Pathophysiology ● B. ECG in Sinus WPW ● C. ECG in AVRT WPW ● D. Presentation ● E. Management ● F. Complications 3. Torsades De Pointes ● A. Pathophysiology ● B. Causes ● C. ECG Findings ● D. Management ● E. Complications 4. Monomorphic Ventricular Tachycardia ● A. Pathophysiology ● B. Causes ● C. ECG Findings 5. Ventricular Fibrillation ● A. Pathophysiology ● B. Causes ● C. ECG Findings

Cardiology: Ventricular Arrhythmias

Bootcamp.com https://commons.wikimedia.org/wiki/File:SVT_Lead_II-2.JPG

SVT •

•

•

Pathophysiology: • Re-entrant pathway within the AV node, accessory pathway, or SA node • Most common = Atrioventricular nodal re-entrant tachycardia (AVNRT) • Second most common = Atrioventricular re-entrant tachycardia (AVRT) Presentation: • Young patient, no significant cardiac history • Abrupt onset, chest pain, dyspnea, palpitations ECG Findings: • Narrow QRS (< 3 little boxes) tachycardia • Heart rate usually >150 beats per minute • P wave may be buried within the QRS complex Management (Stable): • Vagal maneuvers (Carotid sinus massage) • Adenosine • CCBs, β-blockers Management (Unstable): • Electrical cardioversion (Immediate) • Catheter ablation of re-entry pathway (Definitive)

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•

•

AVRT

AVNRT

Atrial T.

Cardiology: Ventricular Arrhythmias

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Bootcamp.com https://commons.wikimedia.org/wiki/File:SVT_Lead_II-2.JPG

•

•

•

• •

•

•

Pathophysiology: • Sinus: Accessory pathway (Bundle of Kent) à bypass AV node (anterograde through bundle of Kent) • Orthodromic AVRT: Re-entrant circuit (anterograde through AV node, retrograde through bundle of Kent) • Antidromic AVRT: Re-entrant circuit (anterograde through bundle of Kent, retrograde through AV node) ECG in Sinus WPW: • Shortened PR interval • Early, “slurred” upstroke of QRS (delta wave) • Wide QRS ECG in AVRT WPW: • Narrow QRS • P wave follows QRS (usually) Presentation: • Sinus: Generally asymptomatic • AVRT: Generally symptomatic Management (Stable): • Procainamide à ideal for antidromic AVRT • Adenosine, CCB à ideal for orthodromic AVRT Management (Unstable): • Electrical cardioversion • Catheter ablation (definitive) Complications: • AV nodal blocking agents and vagal maneuvers à ventricular tachycardia or ventricular fibrillation (unrestricted transmission)

Cardiology: Ventricular Arrhythmias

Bootcamp.com https://commons.wikimedia.org/wiki/File:Tosadesdepointes.jpg

•

Pathophysiology: • Prolonged action potential in cardiomyocytes à Prolonged QT interval à ↑ risk of TdP Causes: • Congenital Long QT Syndrome (usually younger patient)

•

•

• •

Class

Classic Drug

Other Drugs/Effects

A

Antiarrhythmics

Quinidine

Disopyramide, procainamide, sotalol, dofetilide

B

Antibiotics

Macrolides

Fluoroquinolones

C

Antipsychotics

Haloperidol

D

Antidepressants

Tricyclic antidepressants

Methadone

E

Antiemetics/Electrolytes

Ondansetron

Hypocalcemia, hypokalemia, hypomagnesemia

F

Antifungals

Azoles

Ziprasidone AfraTafreeh.com

ECG Findings: • Polymorphic ventricular tachycardia (“twisting of the peaks” pattern) • Irregularly irregular rhythm • Sinusoidal change in amplitude of QRS complexes Management: • Intravenous magnesium • Avoid QT-prolonging medications during acute TdP Complication: • Ventricular fibrillation or sudden cardiac death

Cardiology: Ventricular Arrhythmias

• •

•

• • • • •

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Pathophysiology: • Aberrant ventricular foci • Intraventricular re-entry circuit Causes: • Ischemic and/or structural heart disease • Complication of acute MI • Electrolyte disturbances (hypokalemia, hypomagnesemia) • Acidosis, hypoxemia ECG Findings: • Wide QRS (≥3 little boxes) monomorphic tachycardia • Typically, regular rhythm • Poorly discernible P or T waves at high rates • Heart rates of 100-300 beats per minute

Pathophysiology: • Uncoordinated ventricular depolarization Causes: Similar to Ventricular Tachycardia Association: Cardiac arrest ECG Findings: • Wide QRS (≥3 little boxes) tachycardia • Heart rates of 100-300 beats per minute Complication: • Sudden cardiac death (rapid)

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https://commons.wikimedia.org/wiki/File:Ventricular_fibrillation.png https://commons.wikimedia.org/wiki/File:Lead_II_rhythm_ventricular_tachycardia_Vtach_VT_(cropped).JPG

Ventricular arrhythmias are common in the first 24-48 hours after MI

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A 28-year-old female with a past medical history of alcohol use presents to the emergency department with palpitations and tremors. She denies any chest pain or nausea. The patient states that she recently started using cocaine approximately two months prior. ECG reveals an irregularly irregular rhythm with an erratic baseline, absent P-waves, and an approximate heart rate of 140/min. An intravenous drug is administered. The patient reports becoming very anxious after the drug is given. A cardiac monitoring rhythm strip taken after the patient received the intravenous drug is also shown. The patient subsequently loses consciousness and acute resuscitative measures are initiated. Which of the following intravenous medications were most likely given to this patient?

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⚪ A. Diltiazem ⚪ B. Procainamide ⚪ C. Quinidine ⚪ D. Amiodarone ⚪ E. Ibutilide

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https://commons.wikimedia.org/wiki/File:Ventricular_fibrillation.png

AfraTafreeh.com OUTLINE

1. Atrioventricular Blocks

Cardiology: Conduction Blocks

● A. First Degree ● B. Second Degree, Mobitz Type I (Wenckebach) ● C. Second Degree, Mobitz Type II ● D. Third Degree 2. Bundle Branch Blocks ● A. Right Bundle Branch Blocks ● B. Left Bundle Branch Blocks 3. Cardiac Conduction Blood Supply ● A. Right Coronary Artery ● B. Left Anterior Descending Artery

Cardiology: Conduction Blocks

Bootcamp.com https://en.wikipedia.org/wiki/Heart_block

Asymptomatic •

•

•

•

First Degree: • PR interval >5 little boxes (200ms) • Unchanged P-P intervals • Regular rhythm • Low risk block à Generally conservative management Second Degree, Mobitz Type I (Wenckebach): • Progressive lengthening of PR interval until QRS is dropped • Regularly irregular rhythm • Low risk block à Generally conservative management Second Degree, Mobitz Type II: • Intermittent non-conducted P-waves à dropped QRS • Unchanged P-P intervals • Regularly irregular rhythm • Medium-High risk block à Review medications, pacemaker Third Degree: • Complete AV dissociation (between QRS and P waves) • High risk block à Review medications, pacemaker

High Yield Causes: Ischemic heart disease Hyperkalemia Lyme Disease Endocarditis/ARF

AfraTafreeh.com Iatrogenic

Symptomatic

AV Nodal Blocking Agents Calcium Channel Blockers β-blockers Adenosine Digoxin

Cardiology: Atrioventricular Blocks

•

•

AfraTafreeh.com https://commons.wikimedia.org/wiki/File:Left_bundle_branch_block_ECG_characteristics.svg

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https://commons.wikimedia.org/wiki/File:Right_bundle_branch_block_ECG_characteristics.svg https://commons.wikimedia.org/wiki/File:Cardiogram_indicating_right_bundle_branch_block.jpg https://commons.wikimedia.org/wiki/File:ConductionsystemoftheheartwithouttheHeart-en.svg

Right Bundle Branch Block (RBBB): • Classic causes: Pulmonary embolus, right heart strain, ischemic heart disease • Pseudo-RBBB in Brugada (with ST-elevation in V1-V3) • ”M” shape, “rabbit ears” (Focus on V1) • Slurring of S-wave (Focus on V6) Left Bundle Branch Block (LBBB): • Classic causes: AS, AR, Lyme disease, dilated cardiomyopathy, ischemic heart disease • Lack of R waves (Focus on V1) • Notched R waves (Focus on V6)

Cardiology: Atrioventricular Blocks

•

•

Right Coronary Artery: • SA node • AV node (usually) • Bundle of His (major) • Proximal right bundle branch Left Anterior Descending Artery: • Bundle of His (minor) • Complete left bundle branch • Distal right bundle branch

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A 14-year-old male presents to his pediatrician with his father for shortness of breath and fatigue. He has no significant past medical history although his father has a history of asthma. His father denies any family history of heart disease or sudden cardiac death. The patient states that he has felt “winded” with activity over the past week. According to his father, the shortness of breath became particularly bothersome during football practice. The patient also reports a mild erythematous rash on his forearm that had resolved within three days. The rash was first noticed two weeks earlier when on a hiking trip with family. The patient denies any chest pain, nausea, and diarrhea. Vital signs are shown below. An ECG performed in-office is also shown. Temperature: 99.7F (37.6C) Heart rate: 30/min Blood pressure: 74/44 Respiratory rate: 18/min Oxygen saturation: 94% on room air A drug with which mechanism of action would most likely improve this patient’s condition? ⚪ A. Inhaled short-acting β-agonist ⚪ B. Transient hyperpolarization of cardiac nodal cells ⚪ C. Inhibition of Na+/K+ ATPase in myocardial cells ⚪ D. Inhibition of cardiac L-type calcium channels ⚪ E. Irreversible inhibition of bacterial cell wall synthesis

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OUTLINE 1.

Cardiology: Heart Failure

Heart Failure Overview

● A. Heart Failure Variants of Disease ● B. Heart Failure Location (Left vs Right) ● C. Heart Failure Presentation 2. Systolic Heart Failure ● A. Causes ● B. Pathophysiology 3. Diastolic Heart Failure ● A. Causes ● B. Pathophysiology 4. High and Low Output Heart Failure ● A. Classic Causes 5. Pharmacologic Targets ● A. ACE Inhibitors, ARBs ● B. Mineralocorticoid Receptor Antagonists ● C. β-blockers ● D. Neprilysin Inhibitors ● E. Loop Diuretics ● F. Thiazine Diuretics ● G. Digoxin

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Cardiology: Heart Failure

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Heart Failure Location

Heart Failure Variant • •

• •

Systolic: • Heart failure with reduced ejection fraction (HFrEF) • Principal determinant: ↓ Contractility à ↑↑↑ Volume Diastolic: • Heart failure with preserved ejection fraction (HFpEF) • Principal determinant: ↑↑↑ Pressure à ↓ Compliance High-Output Low-Output

•

•

Left: • • • • Right: • • • • • • • • •

↑ LAP (PCWP) Pulmonary edema Pleural effusion Functional mitral valve regurgitation MCC à Left heart failure If not from left heart failure, unlikely pulmonary edema Hypoxic pulmonary vasoconstriction (Pulmonary HTN) Left parasternal lift Jugular venous distention Peripheral edema Hepatomegaly (Nutmeg liver) Ascites Functional tricuspid valve regurgitation

https://commons.wikimedia.org/wiki/File:Combinpedal.jpg https://commons.wikimedia.org/wiki/File:Pulmonaryedema09.JPG https://commons.wikimedia.org/wiki/File:Normal_posteroanterior_(PA)_chest_radiograph_(X-ray).jpg

Cardiology: Heart Failure

•

•

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Subjective: • Dyspnea with activity (or at rest in severe stages) • Orthopnea • Paroxysmal nocturnal dyspnea Objective • Jugular venous distention • Pulmonary crackles • Reduced Lung Sounds • Shifted PMI (LVH) • Left parasternal lift (RVH) • S3 heart sound • S4 heart sound à classic for diastolic HF • ↑↑↑ BNP

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Cardiology: Heart Failure

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Bootcamp.com https://en.wikipedia.org/wiki/Heart_block

• •

•

Overview: • Heart failure with reduced ejection fraction (HFrEF) • Principal determinant: ↓ Contractility à ↑↑↑ Volume Causes: • Ischemic heart disease • Viral myocarditis • Chronic Alcohol Use Pathophysiology: • ↓ Contractility (↓ EF) à ↓ CO à ↑ LVEDP • Eccentric hypertrophy: ↑ Contractile proteins added in series • ↑ Compliance, ↓ CO, ↓ EF

Cardiology: Heart Failure

Bootcamp.com https://en.wikipedia.org/wiki/Heart_block

• •

•

Overview: • Heart failure with preserved ejection fraction (HFpEF) • Principal determinant: ↑↑↑ Pressure à ↓ Compliance Causes: • Prolonged hypertension • Aortic stenosis • Infiltrative disorders Pathophysiology: • ↑ LVP à ↑ Contractility • Concentric hypertrophy: ↑ Contractile proteins added in parallel • ↓ Compliance, ↓ CO, normal EF Additional Clinical Features: • S4 (due to stiff ventricle)

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•

Cardiology: Heart Failure

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Bootcamp.com https://en.wikipedia.org/wiki/Heart_block

•

Classic Causes: • Thiamine deficiency • Severe anemia • Hyperthyroidism • Arteriovenous fistula

•

Classic Cause: • Cardiogenic shock

Cardiology: Heart Failure

Bootcamp.com https://en.wikipedia.org/wiki/Heart_block

• • • • •

•

• •

ACE Inhibitors (Lisinopril, Captopril, Enalapril, -pril) • Inhibition of ACE à ↓ angiotensin II • Adverse Effect: Dry cough, hyperkalemia, angioedema Angiotensin Receptor Blockers (ARBs) (Valsartan, Losartan, -sartan) • Receptor blockade of angiotensin II type 1 receptor Mineralocorticoid receptor Antagonists (Spironolactone, Eplerenone) β-blockers (Metoprolol, Carvedilol) Neprilysin Inhibitors (Sacubitril): • Neprilysin is a metalloproteinase that inactivates ANP, BNP, and AT-II • ↑ ANP, ↑ BNP, ↑ AT-II • Used with angiotensin-II receptor blocker Loop Diuretic (Furosemide): • Inhibition of Na/K/Cl transporter in ascending limb of loop of Henle • Primary use: Fluid retention and pulmonary edema Thiazide Diuretic (Metolazone): • Inhibition of Na/Cl transporter in distal tubule • Potentiation of loop diuretic effect Digoxin: • Inhibition of Na+/K+-ATPase in myocytes • ↑ Vagal activity to nodal cells • ↑ intracellular calcium concentration in ventricular myocytes • Toxicity: Disturbed color perception, GI symptoms, arrhythmias • Precipitated by hypokalemia

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https://radiopaedia.org/articles/heart-failure-summary?lang=us

A 57-year-old obese female with a past medical history of type II diabetes mellitus, dyslipidemia, chronic hypertension, and coronary artery bypass grafting performed 7 years earlier presents to the emergency department for shortness of breath. She denies any tobacco use and states that she has a glass of wine on rare occasion. She states that she was having difficulty sleeping through the night because she is running to the bathroom every few hours to void. She reports throwing away her ”water pills” last week due to frustration. Blood pressure is 164/88mmHg, heart rate 88/min, respiratory rate 14/min, saturating 94% on 2 liters of oxygen by nasal cannula. Physical exam reveals diffuse crackles bilaterally in the lung fields, an S3 heart sound, and 2+ pitting edema in the bilateral lower extremities. Chest X-ray is shown below. ECG reveals a normal sinus rhythm with mild left ventricular hypertrophy. Thyroid stimulating hormone levels are within normal limits. B-type natriuretic peptide level is significantly elevated. Patient had an echocardiogram performed three months earlier revealing a left ventricular ejection fraction of 30%. Which of the following findings are most consistent with this patient’s acute presentation?

⚪ A. Depressed pulmonary capillary wedge pressure ⚪ B. Depressed central venous pressure ⚪ C. Elevated cardiac index ⚪ D. Increased urinary potassium excretion ⚪ E. Significantly decreased serum levels of vitamin B1

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OUTLINE

Cardiology: Cardiomyopathy

1.

Cardiomyopathy Overview

● ● 2. ● ● ● 3. ● ● ● 4. ● ● ● ● 5. 6. 7. 8. 9. 10.

A. Major Types of Cardiomyopathy B. Cardiac Myocyte Histology Dilated Cardiomyopathy A. Pathophysiology B. Systolic Heart Failure B. Other Classic Causes Restrictive Cardiomyopathy A. Pathophysiology B. Infiltrative Disease C. Diastolic Heart Failure Hypertrophic Obstructive Cardiomyopathy A. Pathophysiology B. Classic Causes C. Histopathology D. Management Viral Myocarditis Chagas Disease Takotsubo Cardiomyopathy Amyloid Cardiomyopathy Aging of Cardiomyocytes Other Causes of Cardiomyopathy

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Cardiology: Cardiomyopathy

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Dilated Cardiomyopathy: • Association with Systolic HF Restrictive Cardiomyopathy: • Association with Diastolic HF Hypertrophic Obstructive Cardiomyopathy • Normal contractility • ↓ Ventricular cavity size • Impaired diastolic function • Septal hypertrophy

Histology of Cardiomyocytes: • Central appearing nuclei • Striation's present • Branching cardiomyocytes

https://commons.wikimedia.org/wiki/File:Blausen_0470_HeartWall.png AfraTafreeh.com https://commons.wikimedia.org/wiki/File:414c_Cardiacmuscle.jpg https://commons.wikimedia.org/wiki/File:Tipet_e_kardiomiopative.png

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Cardiology: Cardiomyopathy

Bootcamp.com https://commons.wikimedia.org/wiki/File:Tipet_e_kardiomiopative.png

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Pathophysiology Systolic Heart Failure: • Eccentric hypertrophy • ↑ Contractile proteins added in series • ↑ LV mass, ↑ LV cavity, ↓ LV EF, Normal LV relaxation Highest Yield Causes: • Systolic heart failure • Viral myocarditis • Chaga’s Disease • Takotsubo Additional Causes: • Familial (AD, truncating mutation of TTN gene) • Pregnancy • Anthracyclines (doxorubicin) • Excess alcohol use • Selenium deficiency

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Cardiology: Cardiomyopathy

AfraTafreeh.com https://commons.wikimedia.org/wiki/File:Tipet_e_kardiomiopative.png

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Pathophysiology Diastolic Heart Failure: • Concentric hypertrophy • ↑ Contractile proteins added in parallel • ↑ LV mass, ↓ LV cavity, Normal/↓ LV EF, ↓ LV relaxation Pathophysiology Restrictive Cardiomyopathy: • Stiffened ventricular walls, not typically thickened (exceptions exist: Amyloidosis) • Normal LV mass, Normal or ↓ LV cavity, Normal LV EF, ↓ LV relaxation Highest Yield Causes: • Diastolic heart failure à Prolonged hypertension, Aortic stenosis • Infiltrative disorders à Amyloidosis, hemochromatosis, sarcoidosis • Radiation-induced Infiltrative Disease Considerations: • Variable ventricular wall thickness (vs hypertensive secondary cause) • Prominent y-descent • Conduction abnormalities

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Cardiology: Cardiomyopathy

https://commons.wikimedia.org/wiki/File:HCM%EF%BC%BFHE.jpg https://commons.wikimedia.org/wiki/File:Tipet_e_kardiomiopative.png

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Pathophysiology: • Genetic mutations of cardiac sarcomere à • β-myosin heavy chain and myosin-binding protein C • Autosomal dominant (most cases) • Dynamic LV outflow tract obstruction (↑ LV septal thickness) • ↑ LV mass, ↓ LV cavity, Normal/↑ LV EF, ↓ LV relaxation Classic Case: • Generally asymptomatic until strenuous exercise • Sudden cardiac death, young patient • Systolic crescendo-decrescendo murmur at LLSB +/- holosystolic murmur at apex • Valsalva à ↓ LV blood volume à Worsen obstruction à ↑ ejection murmur • Passive leg raise à ↑ LV blood volume à Improve obstruction à ↓ ejection murmur • S4 heart sound Histopathology: • Myofibrillary disarray and interstitial fibrosis Mitral Valve: • Anterior mitral leaflet in closer proximity to aortic valve • Distorted mitral valve à ejection against valve à functional mitral regurgitation Management: • Avoid dehydration and strenuous exercise • β-blockers

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Cardiology: Cardiomyopathy

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Bootcamp.com https://en.wikipedia.org/wiki/Heart_block

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Pathophysiology: • Direct viral-induced cytotoxic effect to myocardial cells • Dilated cardiomyopathy (usually) Etiology: • Coxsackievirus • Adenovirus • Influenza virus Classic Case: • Young patient + viral prodrome Histopathology: • Irregular banding patterns, less nuclei observed • Inflammatory infiltration with lymphocytes Primary Cardiomyopathy Subtype: • Dilated cardiomyopathy

Cardiology: Cardiomyopathy

https://www.wikidoc.org/index.php/File:Heart_in_Chagas_disease_4.jpg

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https://en.wikipedia.org/wiki/Heart_block

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Pathophysiology: • Direct parasitic-induced cytotoxic effects Etiology: • Trypanosoma cruzi (Reduviid family) Classic Case: • Central and South America Histopathology: • Protozoa peripheral to myocytes • Inflammatory infiltration with lymphocytes Primary Cardiomyopathy Subtype: • Localized apical wall thinning and/or aneurysm • ↑ risk of mural thrombus and/or emboli • Dilated cardiomyopathy Other Features: • Megaesophagus • Megacolon

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Cardiology: Cardiomyopathy

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Bootcamp.com https://en.wikipedia.org/wiki/Heart_block

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Pathophysiology: • Catecholamine surge à impaired kinetic activity of left ventricle Etiology: • Emotional stress is classic Classic Case: • Death of a loved one • Postmenopausal female Primary Cardiomyopathy Subtype: • Ballooning of left ventricle • Dilated cardiomyopathy

Cardiology: Cardiomyopathy

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https://www.flickr.com/photos/euthman/377559955/ licensed under CC BY-SA 2.0 https://commons.wikimedia.org/wiki/File:Cardiac_amyloidosis_high_mag_he.jpg

Pathophysiology: • ↑ Extracellular deposition of amyloidogenic proteins • Transthyretin (ATTR) • Light chain (AL) Histopathology: • Pink amorphous material surrounding cardiomyocytes • Apple-green birefringence with polarized light and Congo red stain Primary Cardiomyopathy Subtype: • Restrictive cardiomyopathy (Ventricular wall thickening) Other Features of Amyloidosis: • Nephrotic syndrome • Hepatomegaly

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Cardiology: Cardiomyopathy

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https://commons.wikimedia.org/wiki/File:Cardiac_myocyte_showing_lipofuscin_pigment.jpg

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Gross Anatomical Changes: • Sigmoidal shape of ventricular septum Histopathology: • Myofibrillary disarray and interstitial fibrosis • ↑ Lipofuscin pigment • ↑ Connective tissue

Cardiology: Cardiomyopathy

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Hemochromatosis: • ↑ Extracellular deposition of iron • Prussian blue stain (stains iron blue-black) Peripartum/Postpartum: • Dysfunctional angiogenic growth factors • Third trimester peripartum female – postpartum female Anthracycline-Induced • Anthracyclines: Daunorubicin, doxorubicin • Binds with topoisomerase II à cleaves DNA in cancer cells • ↑ with cumulative dose • Prevent with dexrazoxane Trastuzumab-Cardiotoxicity • Monoclonal antibody binding to human epidermal growth factor receptor-2 (HER2) • Does not change with cumulative dose • Tends to be reversible

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A 17-year-old male presents to the emergency room for 8/10 chest pain that began during a soccer practice a few hours earlier. He states that he has experienced chest discomfort and shortness of breath in the past with sports activity and had previously been diagnosed with asthma 3 years earlier. He states that he finds little improvement in his symptoms when using his albuterol inhaler. He denies any other past medical or surgical history. He states that his father and first cousin are both deceased from “heart problems” in their early thirties. He states that he vapes occasionally and denies any other substance use. Blood pressure is 108/58 mmHg, heart rate is 76/min and regular, oxygen saturation is 99% on room air. The point of maximal impulse appears to be modestly shifted laterally beyond the midclavicular line. A 2/6 crescendo-decrescendo systolic murmur is auscultated at the lower left sternal border. The murmur is accentuated with standing. Pulmonary auscultation reveals clear lung sounds bilaterally with no wheezing observed. ECG reveals a regular rhythm with left axis deviation and deep Q waves in leads I, II, III, aVF and V5-V6 are observed. A transthoracic echocardiogram and cardiac MRI are performed. The patient is subsequently prescribed a medication and restricted from further sports activity on discharge. Which of the following mechanisms of action would most likely be consistent with the medication given? ⚪ A. Activation of β1-receptors in myocardial cells ⚪ B. Activation of guanylyl cyclase at venous and coronary vessels ⚪ C. Inhibition of Na+/K+ ATPase in myocardial cells ⚪ D. Inhibition of phosphodiesterase-5 enzymes in vascular smooth muscle ⚪ E. Inhibition of Na+/K+/Cl- co-transporters in the loop of Henle ⚪ F. Non-selective inhibition of β-receptors systemically

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OUTLINE 1.

Cardiology: Aortic Disease

Anatomical Considerations

● A. Aorta ● B. Vessel Wall Layers 2. Aortic Dissection ● A. Pathophysiology ● B. Etiology ● C. Presentation ● D. Stanford Classification ● E. Complications ● F. Imaging ● G. Management 3. Aortic Aneurysm ● A. Thoracic vs Abdominal ● B. Pathophysiology ● C. Risk Factors ● D. Presentation ● E. Preventative Management 4. Cardiac Considerations of Marfan Syndrome ● A. Pathophysiology ● B. Cystic Medial Degeneration ● C. Mitral Valve Prolapse ● D. Other Findings 5. Aortic Coarctation ● A. Pathophysiology ● B. Associations ● C. Presentation ● D. Management

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Cardiology: Aortic Disease

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Aorta: • Ascending: Proximal to brachiocephalic artery • Arch of aorta: Between ascending and descending • Descending: Distal to left subclavian artery Vessel Wall Layers: • Luminal: Tunica intima • Middle: Tunica media • Peripheral: Tunica adventitia (externa)

https://commons.wikimedia.org/wiki/File:Gray506.svg https://radiopaedia.org/cases/normal-cta-chest

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Aortic Isthmus: -Traumatic aortic rupture -Coarctation

Cardiology: Aortic Disease

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https://commons.wikimedia.org/wiki/File:Aortic_dissection_(1)_Victoria_blue-HE.jpg https://commons.wikimedia.org/wiki/File:Aortic_dissection_types.jpg

Pathophysiology: • Tear through intima and media à propagation of dissection through media Etiology: • Acquired: Hypertension (#1), trauma, aortic vasculitis • Connective Tissue Disease: Marfan syndrome, Ehlers-Danlos syndrome • Structural Disease: Coarctation of aorta, Bicuspid aortic valve Presentation: • Severe, acute “tearing” retrosternal chest +/- radiating back pain • Asymmetric blood pressure and pulse discrepancies Stanford A: • Location: Ascending aorta and/or descending aorta • Classic origin: Sinotubular junction • Surgical management (usually) Stanford B: • Location: Descending aorta • Classic origin: Left subclavian artery • Medical management (usually) Complications: • Aortic rupture • Aortic regurgitation • Cardiac tamponade • Ischemia

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Cardiology: Aortic Disease

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https://commons.wikimedia.org/wiki/File:DissectionCT.png

https://commons.wikimedia.org/wiki/File:Descending_(Type_B_Stanford)_Aortic_Dissection.PNG https://commons.wikimedia.org/wiki/File:AoDiss_ChestXRay.jpg

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Imaging: • CXR: Widened mediastinum • CT Angiography (Gold standard): Intimal flap • Transesophageal echocardiogram (TEE) for unstable or renal insufficiency Management: • Stanford A à Surgery • Stanford B à β-blocker then vasodilator

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Cardiology: Aortic Disease

https://commons.wikimedia.org/wiki/File:Thoracic_Aortic_Aneurysm.png https://commons.wikimedia.org/wiki/File:AneurysmT.PNG

Aortic Aneurysms • •

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Pathophysiology: • Transmural inflammation à dilation of intima, media, and adventitia General Risk Factors: • Smoking • Atherosclerosis • Old age • Connective tissue disease • Tertiary Syphilis Classic Presentation: • Generally asymptomatic until rupture Presentation in Rupture: • Acute onset, severe tearing/ripping abdominal/back pain • Severe chest/abdominal pain • Hypotension Preventative: • Abdominal ultrasound screening in men aged 65-75 who have ever smoked (USPSTF)

Thoracic

Bootcamp.com Abdominal

Primary Risk Factor

Hypertension

Smoking

Additional Important Risk Factors

Tertiary syphilis Bicuspid aortic valve Connective tissue disease

Atherosclerosis

Classic Symptoms

Chest pain Mid (thoracic) back pain Hoarseness Dysphagia

Low back pain Abdominal bruit Pulsatile abdominal mass

CXR: Widened mediastinum Ascending aorta (classic location)

Abdominal U/S Infrarenal (classic location)

AfraTafreeh.com Other

Cardiology: Aortic Disease

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AfraTafreeh.com https://www.researchgate.net/figure/Pathologic-finding-of-excised-aortic-tissue-A-cystic-medial-necrosis-which-ishttps://creativecommons.org/licenses/by-nc/3.0/ defined_fig4_221683474

Pathophysiology: • Defect in fibrillin-1 • Autosomal dominant Cystic Medial Degeneration of Aorta: • Aortic aneurysmà Aortic root dilation (thoracic) à Aortic regurgitation and/or dissection • Aortic dissection à most common cause of death • Histopathology: Amorphous extracellular deposition into medial wall Mitral Valve Prolapse: • Mid-systolic click at apex Other Findings: • Tall stature, long extremities • Joint hypermobility • Ectopia lentis, upward lens dislocation • Pectus deformity à carinatum, excavatum • Kyphosis, scoliosis • Arachnodactyly

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Cardiology: Aortic Disease

Bootcamp.com https://commons.wikimedia.org/wiki/File:Rib_Notching.jpg

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Pathophysiology: • Juxtaductal narrowing (aortic isthmus) • Pre-ductal: Infantile form (most common) • Post-ductal: Adult form Association: • Turner syndrome • Bicuspid aortic valve • Williams syndrome • Berry aneurysm à ↑ risk of rupture à SAH Clinical Findings + PDA: • Generally asymptomatic Clinical Findings Without PDA: • Harsh systolic murmur at multiple locations (LSB) • Differential cyanosis • Brachial-femoral delay • Lower extremity claudication Imaging: • CXR: Rib notching Management: • Neonates à prostaglandin E1 • Operative repair

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https://radiopaedia.org/articles/aortic-dissection?lang=us

A 63-year-old male with an unknown past medical history presents to the emergency department with 10/10 “rip-roaring” chest pain. The patient states that he was moving his couch when he suddenly experienced acute-onset of severe chest pain. He denies similar pain in the past. He states that he had one episode of emesis prior to arrival and is feeling very nauseous. He admits to a 35-pack-year smoking history. The patient is unable to provide more details due to the pain. Blood pressure is 204/122 mmHg, heart rate is 101/min and regular, respiratory rate is 18/min, and oxygen saturation is 98% on room air. Electrocardiogram reveals sinus tachycardia and evidence of left ventricular hypertrophy with no signs of ST-segment elevation. Relevant imaging is shown below. Based on these findings, the pathologic process observed most likely originated closest to which of the following structures? ⚪ A. Left renal artery ⚪ B. Left subclavian artery ⚪ C. Right subclavian artery ⚪ D. Aortic isthmus ⚪ E. Sinotubular junction

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OUTLINE 1.

Cardiology: Valvular Disease

Overview

● A. Maneuvers ● B. Murmur Grading 2. Aortic Stenosis ● A. Pathophysiology ● B. Presentation ● C. Etiology 3. Aortic Regurgitation ● A. Pathophysiology ● B. Presentation ● C. Etiology 4. Mitral Stenosis ● A. Pathophysiology ● B. Presentation ● C. Etiology 5. Mitral Regurgitation ● A. Pathophysiology ● B. Presentation ● C. Etiology 6. Mitral Valve Prolapse ● A. Pathophysiology ● B. Presentation ● C. Etiology 7. Tricuspid Regurgitation ● A. Pathophysiology ● B. Presentation ● C. Etiology

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Cardiology: Valvular Disease

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↑ Preload • Passive leg raise • Squatting • Expiration: ↓ RV preload, ↑ LV preload à intensifies most left-sided murmurs, dulls most right-sided murmurs ↓ Preload • Valsalva (straining phase) • Standing (from squat or supine) • Inspiration: ↑ RV preload, ↓ LV preload à intensifies most right-sided murmurs, dulls most left-sided murmurs ↑ Afterload: • Hand Grip • Squatting

Systolic vs Diastolic • Systolic may be physiologic • Diastolic almost always pathologic • Continuous murmur (ex. PDA) Grade • I: Detected with very careful auscultation • II: Detected quickly with auscultation • III: Easily heard, with no thrill • IV: Palpable thrill • V: Detected with rim of stethoscope touching chest + palpable thrill • VI: Audible with stethoscope off chest

Cardiology: Valvular Disease

Bootcamp.com https://commons.wikimedia.org/wiki/File:Amyloidosis,_dystrophic_calcification,_H%26E.jpg

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Pathophysiology: • Left ventricular outflow obstruction à ↑ LVP à LV Concentric hypertrophy à DHF à S4 heart sound Presentation: • Classic Triad: Exertional dyspnea, angina, syncope • Pulsus parvus et tardus • Single S2 (or soft S2) • Murmur: Harsh crescendo-decrescendo systolic ejection murmur, radiates to carotids • Murmur Auscultation: R 2nd ICS • ↑ Murmur: ↑ Preload, ↓ Afterload, Expiration Age-related Aortic Valve Sclerosis: • MCC overall • Classically, elderly patients • Earlier presentation if bicuspid aortic valve Bicuspid Aortic Valve: • Fusion of two aortic leaflets in young patients • ↑ risk of premature dystrophic calcification

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Cardiology: Valvular Disease

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Pathophysiology: • Acute: Regurgitant blood into LV à Poor compensation due to rapid physiologic changes • Chronic: Regurgitant blood into LV à ↑ LVEDV à LV eccentric hypertrophy à SHF à S3 heart sound • ↑ Pulse pressure Presentation: • Exertional dyspnea • Pulmonary edema • “Water hammer” pulse • Head bobbing • Murmur: Early decrescendo diastolic murmur • Murmur Auscultation: L 3rd-4th ICS along LSB (Erb’s Point) • ↑ Murmur: ↑ Preload, ↑ Afterload, Expiration Age-related Aortic Valve Sclerosis: • MCC overall • Classically, elderly patients Bicuspid Aortic Valve: • Fusion of two aortic leaflets in younger patients • ↑ risk of dystrophic calcification to valve Aortic Dilatation: • Secondary to: Aortic dissection, aneurysm, connective tissue disease, and/or tertiary syphilis • Chronic poorly controlled hypertension à aortic dissection and thoracic aortic aneurysm Rheumatic Heart Disease

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Cardiology: Valvular Disease

Bootcamp.com https://commons.wikimedia.org/wiki/File:Leg_with_erythema_marginatum_Wellcome_L0061869.jpg

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Pathophysiology: • Left atrial outflow obstruction à ↓ LVEDV, left atrial dilation à ↓ CO Presentation: • Exertional dyspnea • Pulmonary edema • Hoarseness, dysphagia • Loud S1 • Murmur: Opening snap, diastolic “rumbling” murmur • Murmur Auscultation: L 5th ICS midclavicular line (apex) • ↑ Murmur: ↑ Preload, ↓ Afterload, Expiration • Murmur Interval: ↓ time between S2 and OS ~ ↑ disease severity Rheumatic Heart Disease: • Most common cause overall • Manifestations years after acute rheumatic fever Complications: • Atrial fibrillation

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• •

Acute Rheumatic Fever Presentation Acute/Subacute: Migratory arthritis Pancarditis à mitral prolapse/regurgitation Sydenham chorea Subcutaneous nodules Erythema marginatum Chronic: Mitral Stenosis

Cardiology: Valvular Disease

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Pathophysiology: • Acute: Regurgitant blood into LA à ↑ PCWP à Poor compensation due to rapid physiologic changes • Chronic: Regurgitant blood into LA à ↑ LVEDV à LV eccentric hypertrophy à SHF à S3 heart sound Presentation: • Exertional dyspnea • Pulmonary edema • Hoarseness, dysphagia • Soft S1 • Murmur: Holosystolic “blowing” murmur • Murmur Auscultation: L 5th ICS midclavicular line (apex) • ↑ Murmur: ↑ Preload, ↑ Afterload, Expiration Association: • Papillary muscle rupture • Mitral valve prolapse • Infective endocarditis à Mitral valve (#1) Complication: • Atrial fibrillation

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Cardiology: Valvular Disease

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Pathophysiology: • Myxomatous degeneration of mitral valve à ↑ tension on chordae tendineae and papillary muscles Presentation: • Generally asymptomatic • Murmur: Mid-systolic click, late systolic crescendo murmur • Murmur Auscultation: L 5th ICS midclavicular line (apex) • ↑ Murmur: ↓ Preload, Expiration • Later click with ↑ afterload Association: • Connective tissue disease (Marfan Syndrome) • Papillary muscle rupture • Infective endocarditis à Mitral valve (#1) • Rheumatic heart disease Complication: • Atrial fibrillation • Recurrence of infective endocarditis

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Cardiology: Valvular Disease

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Pathophysiology: • Acute: Regurgitant blood into RA à ↑ CVP à Poor compensation due to rapid physiologic changes • Chronic: Regurgitant blood into RA à Right-sided heart failure Presentation: • Distended jugular veins • Hepatomegaly • Ascites • Peripheral edema • Murmur: Holosystolic murmur • Murmur Auscultation: 4th ICS LLSB • ↑ Murmur: ↑ Preload, ↑ Afterload, Inspiration Association: • Infective endocarditis in IVDU à septic pulmonary emboli • Carcinoid syndrome

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Cardiology: Valvular Disease

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Valvular Disease

Murmur

Auscultation Location

Unique Feature

Classic Cause

Heart Failure

↑ Murmur Intensity

Aortic Stenosis

Holosystolic crescendodecrescendo

2nd R ICS

Radiation to carotids

Dystrophic calcification

Diastolic: Concentric hypertrophy (S4)

↑ Preload (Passive leg raise) ↓ Afterload

Aortic Regurgitation

Diastolic decrescendo murmur

Erb’s point

High pulse pressure

Multiple

Systolic: Eccentric hypertrophy (S3)

↑ Preload (Passive leg raise) ↑ Afterload (Hand grip)

Mitral Stenosis

Diastolic decrescendo murmur

Cardiac apex

Opening snap

Rheumatic heart disease

Low output

↑ Preload (Passive leg raise) ↓ Afterload

Mitral Regurgitation

Holosystolic murmur

Cardiac apex

Radiate to axilla

Mitral valve prolapse

Systolic: Eccentric hypertrophy (S3)

↑ Preload (Passive leg raise) ↑ Afterload (Hand grip)

Mitral Valve Prolapse

Late-systolic crescendo murmur

Cardiac apex

Mid-systolic click

Multiple

Mitral regurgitation à Systolic

↓ Preload (Valsalva) Later click with ↑ Afterload

Tricuspid Regurgitation

Holosystolic murmur

4th L ICS

↑ with inspiration

IVDU à Infective endocarditis

Right-sided

↑ with Inspiration ↑ Preload (Passive leg raise) ↑ Afterload (Hand grip)

Hypertrophic Obstructive Cardiomyopathy

Systolic crescendodecrescendo murmur

Left lower sternal border

Young patient

Inherited mutations in sarcomere

Septal hypertrophy (S4)

↓ Preload (Valsalva) ↓ Afterload

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https://commons.wikimedia.org/wiki/File:AP_portable_CXR_of_a_patient_in_acute_pulmonary_oedema.jpg

A 67-year-old male with a past medical history of obstructive sleep apnea, tobacco use, chronic hypertension, and hyperlipidemia presented to the emergency department with acute onset of severe chest pain. Vital signs on arrival were significant for a blood pressure of 94/58 mmHg, heart rate 102/min, respiratory rate 14/min, and oxygen saturation of 98% on room air. Electrocardiogram revealed ST-segment depression and tall R-waves in leads V2, V3, and V4. Chest x-ray was unremarkable. Percutaneous coronary intervention with stent placement was performed which disclosed severely obstructing stenosis in the ostium of the posterior descending artery. On day 3 of admission, the patient develops acute dyspnea while lying in bed with 3/10 non-specific chest pain. Blood pressure is 184/110 mmHg and a new 3/6 “blowing” holosystolic murmur is auscultated at the cardiac apex radiating into the left axilla. Chest x-ray is shown below. A medication is administered, and the patient’s murmur becomes softer and more difficult to auscultate. Which of the following mechanisms of the unknown medication would be most likely responsible for decreasing the murmur intensity in this patient? ⚪ A. Increased intracellular cGMP activity at arterioles and venules ⚪ B. Increased intracellular phospholipase C activity at arterioles and venules ⚪ C. Increased intracellular cAMP activity at cardiac myocytes ⚪ D. Decreased intracellular cAMP activity at arterioles and venules ⚪ E. Decreased intracellular Na+/K+-ATPase activity at cardiac myocytes

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OUTLINE 1.

Cardiology: Acyanotic Congenital Heart Defects

Overview

● A. Acyanotic ● B. Cyanotic ● C. Symptomatic Patient ● D. General Diagnostics 2. Ventricular Septal Defect ● A. Pathogenesis ● B. Pathophysiology ● C. Presentation ● D. Diagnostics ● E. Association 3. Atrial Septal Defect ● A. Pathogenesis ● B. Pathophysiology ● C. Presentation ● D. Diagnostics ● E. Association 4. Patent Foramen Ovale ● A. Pathogenesis ● B. Pathophysiology ● C. Presentation ● D. Diagnostics

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5.

Patent Ductus Arteriosus

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A. Pathogenesis B. Pathophysiology C. Presentation D. Diagnostics E. Management F. Association Eisenmenger Syndrome A. Pathophysiology B. Presentation

Cardiology: Acyanotic Congenital Heart Defects

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Acyanotic • Left à Right shunting • Tends to be later presentation overall • 3 D’s: ASD, VSD, PDA Cyanotic • Right à Left shunting • Early presentation (shortly after birth) • Cyanotic Presentation: Blue skin discoloration, mucosal cyanosis, failure to thrive, dyspnea • 5 T’s: Tetralogy of Fallot, TAPVR, Truncus Arteriosus, Tricuspid Valve Atresia, Transposition of Great Vessels General Presentation of Symptomatic Patient: • Tachypnea • Failure to thrive • Cyanosis à Cyanotic CHD, Eisenmenger syndrome • Recurrent bronchopulmonary infections à Acyanotic Diagnostics: • Echocardiography à Confirmatory test • Bubble study à Useful in detecting RàL shunts

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Cardiology: Acyanotic Congenital Heart Defects

Bootcamp.com https://commons.wikimedia.org/wiki/File:Vsd_simple-lg.jpg

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Pathogenesis: • Defect in membranous part of ventricular septum (most common) Pathophysiology: • Left à Right shunting through defect in interventricular septum • RV volume overload à Presentation: • Harsh holosystolic murmur, LLSB • ↓ Murmur à ↑ Severity/Size • Usually at 2-3 months in severe disease (vs most cyanotic) Diagnostics: • Echocardiography à Confirmatory test Association: • Down syndrome • Maternal diabetes

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Cardiology: Acyanotic Congenital Heart Defects

AfraTafreeh.com https://commons.wikimedia.org/wiki/File:Asd-web.jpg

• •

•

• •

Pathogenesis: • Defect in inter-atrial septum, ostium secundum defect (most common) Pathophysiology: • Left à Right shunting through defect of atrial septum • Valsalva à ↑ RAP with subsequent Right à Left shunting Presentation: • Classically, adolescent or adult • Wide fixed split S2 • Paradoxical embolism à Cryptogenic stroke Diagnostics: • Echocardiography à Confirmatory test Association: • Down syndrome • Fetal alcohol syndrome • Holt-Oram syndrome

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Cardiology: Acyanotic Congenital Heart Defects

Bootcamp.com https://commons.wikimedia.org/wiki/File:Foramen_ovale.png

• •

• •

Pathogenesis: • Impaired fusion of septum primum and septum secundum Pathophysiology: • Left à Right shunting through defect of atrial septum • Valsalva à ↑ RAP with subsequent Right à Left shunting Presentation: • Usually, asymptomatic • Paradoxical embolism à Cryptogenic stroke Diagnostics: • Echocardiography à Confirmatory test

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Cardiology: Acyanotic Congenital Heart Defects

AfraTafreeh.com https://commons.wikimedia.org/wiki/File:Patent_ductus_arteriosus.svg

• •

•

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•

Pathogenesis: • Impaired closure of ductus arteriosus • Derived from sixth, left aortic arch Pathophysiology: • Left à Right shunting from aorta to pulmonary vessels • Prostaglandins and low oxygen tension à maintain PDA Presentation: • Continuous “machine-like” murmur, left infraclavicular region • Usually, asymptomatic if mild case • Severe cases more likely to be symptomatic • Wide pulse pressure (similar to AR) Diagnostics: • Echocardiography à Confirmatory test Management: • Premature symptomatic infant à Indomethacin à Close PDA • Cyanotic congenital heart defect à Prostaglandin E1 (Alprostadil) à Maintain PDA Association: • Prematurity • Rubella (first trimester) • Fetal alcohol syndrome • Fetal hydantoin syndrome

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Cardiology: Acyanotic Congenital Heart Defects

•

•

Pathophysiology: • Shunt reversal • Pulmonary vessel sclerosis • Chronic L to R shunting à pulmonary hypertension à RVH à RVP > LVP à R to L shunting Presentation: • Cyanosis • Fingernail clubbing • Heart failure • Differential cyanosis and clubbing with PDA

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A 9-month-old female with known Trisomy 21 presents with her mother with a chief complaint of progressively worsening difficulty breathing and a new nonproductive cough that started approximately one month earlier. Her mother reports the symptoms are most noticeable when breastfeeding. Physical examination reveals a respiratory rate of 52/min with otherwise stable vital signs, upslanting palpebral fissures, low set ears, perioral cyanosis, and mild nasal flaring. Bronchial breath sounds and a heart murmur are auscultated. Chest X-ray reveals diffuse patches of opacification and cardiomegaly. An echocardiogram is performed and followed by a cardiac catheterization procedure. Oxygen saturation by cardiovascular location is listed below. Which of the following most likely describes the cause of this patient’s presentation? Superior vena cava: SpO2 68% Inferior vena cava: SpO2 70% Right atrium: SpO2 69% Right ventricle: SpO2 69% Left atrium: SpO2 98% Left ventricle: SpO2 87% Pulmonary artery : SpO2 69% Pulmonary vein: 98% ⚪ A. Long-term exogenous prostaglandin exposure ⚪ B. Atrial septal tissue deficiency ⚪ C. Impaired fusion of septum primum and secundum ⚪ D. Reversal of atrial shunt ⚪ E. Reversal of ventricular shunt

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OUTLINE 1.

Cardiology: Cyanotic Congenital Heart Defects

Overview

● A. Acyanotic ● B. Cyanotic ● C. Symptomatic Patient ● D. General Diagnostics 2. Tetralogy of Fallot ● A. Pathogenesis ● B. Pathophysiology ● C. Presentation ● D. Diagnostics ● E. Management ● F. Associations 3. Transposition of Great Vessels ● A. Pathogenesis ● B. Pathophysiology ● C. Presentation ● D. Diagnostics ● E. Management ● F. Association 4. Persistent Truncus Arteriosus ● A. Pathogenesis ● B. Pathophysiology ● C. Presentation ● D. Diagnostics ● E. Association

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5.

Tricuspid Atresia

● ● ● ● ● ● 6. ● ● ● ● ● ●

A. Pathogenesis B. Pathophysiology C. Presentation D. Diagnostics E. Management F. Association TAPVR A. Pathogenesis B. Pathophysiology C. Presentation D. Diagnostics E. Management F. Associations

Cardiology: Acyanotic Congenital Heart Defects

•

•

•

•

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Acyanotic • Left à Right shunting • Tends to be later presentation overall • 3 D’s: ASD, VSD, PDA Cyanotic • Right à Left shunting • Early presentation (shortly after birth) • Cyanotic Presentation: Blue skin discoloration, mucosal cyanosis, failure to thrive, dyspnea • 5 T’s: Tetralogy of Fallot, TAPVR, Truncus Arteriosus, Tricuspid Valve Atresia, Transposition of Great Vessels General Presentation of Symptomatic Patient: • Tachypnea • Failure to thrive • Cyanosis à Cyanotic CHD, Eisenmenger syndrome • Recurrent bronchopulmonary infections à Acyanotic Diagnostics: • Echocardiography à Confirmatory test • Bubble study à Useful in detecting RàL shunts

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Cardiology: Cyanotic Congenital Heart Defects

https://commons.wikimedia.org/wiki/File:Heart_tetralogy_fallot.svg https://commons.wikimedia.org/wiki/File:Boot-shaped_heart.jpg

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•

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•

•

Pathogenesis: • Deviation of infundibular septum • A. Pulmonic Stenosis (RVOTO) • B. Overriding aorta • C. Ventricular septal defect (VSD) • D. RV hypertrophy Pathophysiology: • Severity of RVOTO determines blood flow • Mild RVOTO: L à R • Severe RVOTO: R à L Presentation (tachypnea, cyanosis): • Tet spells • Harsh systolic ejection murmur, LUSB Diagnostics: • CXR: Boot-shaped heart • Echocardiography à Confirmatory test Management: • Severe: PGE1 à Surgery • Knee to chest • Oxygen Associations: • DiGeorge syndrome • Down syndrome • Fetal alcohol syndrome

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Hyperoxia Test: 100% O2 administered ~10 minutes Measure PaO2 Pulmonary Dz: ↑↑↑ PaO2

Congenital Heart Dz: -/↑ PaO2

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Cardiology: Cyanotic Congenital Heart Defects

AfraTafreeh.com https://commons.wikimedia.org/wiki/File:D-tga-575px.jpg

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https://commons.wikimedia.org/wiki/File:Transposition-of-great-vessels.jpg

• •

• •

• •

Pathogenesis: • Failed spiraling of aorticopulmonary septum à reversal of pulmonary artery and aorta Pathophysiology: • Two parallel circuits • RVà Aorta • LV à Pulmonary artery Presentation (tachypnea, cyanosis): Diagnostics: • CXR: “Egg-on-a-string” • Echocardiography à Confirmatory test Management: • PGE1 à Surgery • Balloon septoplasty Association: • Maternal diabetes

Cardiology: Cyanotic Congenital Heart Defects

Bootcamp.com https://commons.wikimedia.org/wiki/File:Truncus_arteriosus.jpg

• •

• • • •

Pathogenesis: • Partial (incomplete) aorticopulmonary septum formation • Failure of neural crest cell migration Pathophysiology: • Mixing of oxygenated and deoxygenated blood at the ventricles • Ventricular septal defect Presentation (tachypnea, cyanosis): • Harsh systolic ejection murmur, LLSB Diagnostics: • Echocardiography à Confirmatory test Management: • Surgery Association: • DiGeorge syndrome

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Cardiology: Cyanotic Congenital Heart Defects

AfraTafreeh.com https://commons.wikimedia.org/wiki/File:Tricuspid_atresia.svg

• •

• • • •

Pathogenesis: • Absent tricuspid valve Pathophysiology: • ↓↓↓ Blood to RVà RV hypoplasia, RA dilation • Atrial septal defect Presentation (tachypnea, cyanosis): Diagnostics: • CXR: Cardiomegaly • Echocardiography à Confirmatory test Management: • PGE1 à Surgery Association: • Ebstein Anomaly (Lithium exposure)

*Tetragenic exposure from lithium during early stages of pregnancy is associated with the development of Ebstein Anomaly in the fetus*

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Cardiology: Cyanotic Congenital Heart Defects

https://commons.wikimedia.org/wiki/File:Tapv-575px.jpg

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https://radiopaedia.org/articles/snowman-sign-total-anomalous-pulmonary-venous-return-1?lang=us

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Pathogenesis: • Anomalous pulmonary veins Pathophysiology: • Pulmonary veins à Right heart circulation (rather than LA) • ↑ Pulmonary pressures • Atrial septal defect Presentation (tachypnea, cyanosis): Diagnostics: • CXR: Snowman sign • Echocardiography à Confirmatory test Management: • Surgery

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Cardiology: Cyanotic Congenital Heart Defects

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#

Disease

Principle Problem

Distinguishing Features

Unique CXR Findings

Associations

1

Persistent Truncus Arteriosus

Incomplete aorticopulmonary septum formation à single vessel

Typically, with minimal cyanosis initially

----

DiGeorge Syndrome

2

Transposition of Great Vessels

Failed spiraling of aorticopulmonary septum à aorta and pulmonary artery switched locations

Severe cyanosis at birth Two parallel circuits, requires ASD, PFO, VSD, and/or PDA for survival

Egg-on-a-string

Maternal diabetes

3

Tricuspid Atresia

No functional tricuspid valve, hypoplastic RV

Severe cyanosis at birth Requires ASD, PFO, VSD, and/or PDA

↓ Pulmonary markings

Ebstein Anomaly (Lithium)

4

Tetralogy of Fallot

Deviation of infundibular septum, pulmonic stenosis, overriding aorta, RVH, VSD

Tet spells

Boot-shaped heart

DiGeorge syndrome Down syndrome Maternal alcohol use

5

Total Anomalous Pulmonary Venous Return

Pulmonary veins drain into right heart circulation

Pulmonary hypertension

Snowman sign

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A 24-year-old male with a past medical history of bipolar type I disorder who presents to the emergency department with a 3week history of palpitations and dyspnea. He states that his symptoms occur sporadically with no clear trigger and last up to 30 minutes at a time. He denies any tobacco or illicit drug use and states that he has a glass of wine every weekend. Vital signs include a temperature of 98.4F (36.9C), blood pressure of 110/88, heart rate of 66/min, and a respiratory rate of 12/min. Physical examination reveals a 2/6 holosystolic murmur at the left sternal border. The murmur is accentuated with deep inspiration. Electrocardiogram is shown below. Transthoracic echocardiography is performed. Which of the following imaging findings would most likely be consistent with this patient’s initial presentation?

AfraTafreeh.com ⚪ A. Right ventricular outflow tract obstruction ⚪ B. Right ventricular atrialization ⚪ C. Right ventricular structural attachment to aorta ⚪ D. Malpositioning of pulmonic veins ⚪ E. Single outflow vessel from right and left ventricles

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https://commons.wikimedia.org/wiki/File:E204_(CardioNetworks_ECGpedia).jpg

AfraTafreeh.com OUTLINE

Cardiology: Stable Angina and Atherosclerosis

1. Arterial Disease

5.

Chest Pain DDx

● A. Atherosclerosis ● B. Mönckeberg Arteriosclerosis ● C. Arteriosclerosis 2. Atherosclerosis ● A. Pathogenesis ● B. Location ● C. Risk Factors ● D. Complications 3. Plaque Stability ● A. Stable ● B. Unstable 4. Coronary Artery Disease ● A. Angina Terminology ● B. Variant Disease 5. Stable Angina ● A. Pathogenesis ● B. Pathophysiology ● C. Presentation ● D. Diagnostics ● E. Medical Management 6. Vasospastic Angina ● A. Pathophysiology ● B. Presentation ● C. Diagnostics ● D. Associations ● E. Management

6. ● ● ● ●

Anti-anginal Therapy A. Nitrates B. β-blockers C. Calcium Channel Blockers D. Ranolazine

Cardiology: Stable Angina and Atherosclerosis

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•

https://commons.wikimedia.org/wiki/File:Moenckeberg.jpg https://commons.wikimedia.org/wiki/File:Blausen_0055_ArteryWallStructure.png https://commons.wikimedia.org/wiki/File:%22Onion-skin%22_renal_arteriole.jpg https://commons.wikimedia.org/wiki/File:Renal_arterial_hyalinosis_-_pas_-_very_high_mag.jpg

Atherosclerosis • Cholesterol plaque accumulation within vessel walls • Intima classically involved Mönckeberg Arteriosclerosis • Dystrophic calcification within vessel walls • Media classically involved • Lumen unaffected Arteriolosclerosis: • Response to ↑ pressure • Hyaline à pink amorphous deposits in arterial wall • Hyperplastic à “Onion-skin” appearance

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Cardiology: Stable Angina and Atherosclerosis

•

• •

•

AfraTafreeh.com https://commons.wikimedia.org/wiki/File:CT_image_of_atherosclerosis_of_the_abdominal_aorta.svg https://commons.wikimedia.org/wiki/File:Late_complications_of_atherosclerosis.PNG

Pathogenesis: • Endothelial stress à Dysfunction à Subendothelium exposure à Platelet binding à PDGF and cytokine release • Monocyte's adhesion à Macrophages activated in vessel intima • Smooth muscle cells recruited to intima via PDGF, FGF, endothelin-1, interleukin-1 • Macrophage and smooth muscle cell digestion of lipids (LDL) à Foam cells à Fatty streak • Smooth muscle cell proliferation, deposition of extracellular matrix à Fibrous cap formation • Fibrous atheroma (plaque) à Complex atheroma (calcification) Location: • Abdominal aorta > Coronary artery > Popliteal artery > Carotid artery > Circle of Willis Risk Factors: • Smoking • Diabetes mellitus • Hypertension • Dyslipidemia (↑ LDL) • Age Complications: • Obstructive plaque à At risk for local vascular occlusion • Plaque rupture à Thrombus at risk of vascular occlusion • Aneurysm and rupture

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Cardiology: Stable Angina and Atherosclerosis

•

•

Stable Atherosclerotic Plaque: • Progressive ↓ coronary blood flow • ↑ growth factor release (ex. VEGF) • Collateral circulation Unstable Atherosclerotic Plaque: • Chronic inflammation à Macrophage activation à • Metalloproteinases break down extracellular matrix proteins à Thin-cap fibroatheromas • ↑ Risk of rupture à Rupture à Thrombus formed over plaque à Acute coronary syndrome

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Cardiology: Stable Angina and Atherosclerosis

•

• •

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Typical Angina: Requires all 3 criteria below are met • Retrosternal chest pain • Worsened with exertion or emotional stress • Improved with rest or nitroglycerin Atypical Angina: 2 out of 3 criteria are met Nonanginal: Less than 2 out of 3 criteria are met

Coronary Artery Disease

• • • • •

Stable Angina: Atherosclerotic lesion, >70% stenosis Vasospastic Angina: Hyperactive vascular smooth muscle Unstable Angina: Atherosclerotic lesion, partially obstructive thrombus NSTEMI: Atherosclerotic lesion, partially obstructive thrombus STEMI: Atherosclerotic lesion, completely obstructive thrombus

Acute Coronary Syndrome

Angina

Stable Angina Vasospastic Angina

Unstable Angina

NSTEMI

STEMI

Cardiology: Stable Angina and Atherosclerosis

•

Pathogenesis: • Fixed stenosis of coronary vessel (>70%) without tissue infarction Pathophysiology: • Atherosclerotic disease (usually) à ↓ Coronary perfusion • Temporary oxygen supply-demand mismatch with activity • Presentation: • Reproducible symptoms with activity • ↑ Symptoms with ↑ myocardial oxygen demand à Exercise, dobutamine • ↓ Symptoms with ↓ myocardial oxygen demand à Rest, nitroglycerin • Classic chest pain: Retrosternal, radiating, non-pleuritic, non-reproducible to palpation • Other: Chest pressure, tightness, squeezing • Diagnostics: Stress testing • Exercise à ↑ Myocardial O2 demands • Pharmacologic à Dobutamine, Dipyridamole, Adenosine à ↑ Myocardial O2 demands • ECG used to evaluate for acute ST changes • Echocardiography or myocardial perfusion scan can also be utilized Cardiac angiography ECG à No significant ST-changes Cardiac enzymes à Not significantly elevated • Medical Management: • Antianginal therapy à Nitrates à Symptomatic relief • Antiplatelet therapy à Aspirin or Clopidogrel à ↓ Risk of occlusive thrombus formation • Statin therapy à Atorvastatin à ↓ Risk of acute coronary events • Antihypertensive therapy (if applicable) à ACE inhibitor, ARB

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Cardiology: Stable Angina and Atherosclerosis

• •

•

•

•

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Pathophysiology: • Transient, spontaneous coronary vasospasms Presentation: • Recurrent chest pain/discomfort, resolving with minutes • Classically occurring at night (↑ vagal tone) • Not affected by exertion • Younger patient, usually lacking risk factors for CAD (exception smoking) Diagnostics: • ECG: ST-segment elevation with an episode • -- Symptoms à Rest • ↓ Symptoms à Nitroglycerin Associations: • Tobacco use • Cocaine • Amphetamines • Triptans, Ergot alkaloids • Alcohol Management: • Acute à Nitroglycerin • Preventative à Avoid precipitating factors (ex. smoking), calcium channel blockers

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Cardiology: Stable Angina and Atherosclerosis

•

•

Nitrates • Nitroglycerin (Sublingual à rapid effect) • Isosorbide Dinitrate • ↑ cGMP à peripheral and coronary vasodilation à ↓ preload, ↑ myocardial perfusion • Right Ventricular MI: Avoid agents that ↓ preload • Nitrate Tolerance: Maintain nitrate free intervals • Adverse Effects: Hypotension, flushing, headaches • Avoid with concomitant use of PDE-5 inhibitors (ex. Sildenafil) β-blockers • Metoprolol • ↓ cAMP à ↓ intracellular Ca2+ • β-Blocker Withdrawal Syndrome: ↑ HR, contractility à Angina, following discontinuation of β-blocker therapy • Avoid in the setting of AV block Nondihydropyridine Calcium Channel Blockers • Verapamil, Diltiazem • ↓ Binding to calcium channels à ↓ intracellular Ca2+ • Avoid in setting of AV block Ranolazine • Inhibition of late inward sodium channels à ↓ Ca2+ influx à ↓ intracellular Ca2+ • Adverse Effects: QT prolongation

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•

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https://commons.wikimedia.org/wiki/File:Histopathology_of_progressive_atherosclerotic_lesions.jpg

A 69-year-old obese male with an unknown past medical history is rushed to the emergency department by friends after being found unconscious in the bathroom. The patient and his friends were playing a poker game, drinking alcohol, smoking cigarettes, and eating pizza. The patient left the room to use the bathroom and had not returned for approximately 45 minutes. He was found face down on the floor, unconscious and unresponsive. The patient regained consciousness intermittently en route to the emergency department with EMS during CPR. The patient was hemodynamically unstable on arrive despite inotropic agents. Within minutes of arrival, he went into an episode of cardiac arrest and subsequently expired. Autopsy performed revealed a complete thrombotic occlusion of the left main coronary artery. Several atheroma's were identified throughout the coronary vasculature. A histological section is analyzed. A fibrous cap (FC) atheroma with a well-formed necrotic core (NC) is observed and shown below. Which of the following cell types are most directly responsible for the formation of FC? ⚪ A. Foam cells ⚪ B. Monocytes ⚪ C. Macrophages ⚪ D. Smooth muscle cells ⚪ E. Endothelial cells

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OUTLINE 1.

Cardiology: Myocardial Infarction

Overview

● A. Unstable Angina ● B. NSTEMI ● C. STEMI 2. Myocardial Infarction ● A. Pathogenesis ● B. Pathophysiology ● C. Left Ventricular Dysfunction ● D. Right Ventricular Dysfunction ● E. Myocardial Stunning ● F. Myocardial Hibernation ● G. Reperfusion Injury 3. Post-MI Timeline ● A. Acute Phase ● B. Inflammatory Phase ● C. Proliferative Phase ● D. Remodeling Phase 4. ECG Localization in STEMI ● A. Infarct Age ● B. ST-Elevations ● C. Lead Localization 5. Cardiac Biomarkers ● A. Troponin ● B. CK-MB

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6. ● ● ● ● ● ●

Management A. Statin B. Antiplatelet C. Glycoprotein IIb/IIIa Inhibitor D. Anticoagulation E. Thrombolytics F. Percutaneous Coronary Intervention

Cardiology: Myocardial Infarction

AfraTafreeh.com https://commons.wikimedia.org/wiki/File:Heart_attack-NIH.gif

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Unstable Angina: • Atheromatous plaque rupture à Incomplete occlusion à No appreciable infarction • ECG: T wave and ST-segment abnormalities are possible, no ST-elevation • Cardiac biomarkers are not significantly elevated NSTEMI: • Atheromatous plaque rupture à Incomplete occlusion à Subendocardial infarction • ECG: T wave and ST-segment abnormalities are possible, no ST-elevation • Cardiac biomarkers are significantly elevated STEMI: • Atheromatous plaque rupture à Complete occlusion à Transmural infarction • ECG: Peaked T-waves à ST-elevation (minutes) à deep Q-waves (hours) • New LBBB can be suggestive of STEMI • Cardiac biomarkers may be significantly elevated

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Cardiology: Myocardial Infarction

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•

• • •

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Pathogenesis: • Complete occlusion (usually) of coronary vessel (LAD most common) • Atheromatous plaque rupture is classic à Acute thrombus occludes vessel lumen Pathophysiology • ↓ Aerobic metabolism à ↑ Anaerobic metabolism à ↑ Lactate, ↓ ATP (Reversible if rapid reperfusion) • ↓ Contractility due to ischemic insult à Heart failure, cardiogenic shock Left Ventricular Dysfunction: • Anterolateral MI à Leads I, aVL, V1-V6 • Supply: Left main, LCX and/or LAD • ↓ Contractility à ↓ Cardiac outputà Cardiogenic shock • Left-sided heart failure à ↑ PCWP à PHTN à Pulmonary edema à ↑ CVP Right Ventricular Dysfunction • Inferior wall MI à Leads II, III, aVF • Supply: Posterior descending artery (RCA in right-dominant circulation) • Right-sided heart failure à Preload-dependency, ↑ CVP in setting of normal or ↓ PCWP • Avoid ↓ preload if possible (venodilators, diuresis) • Electrical conductivity defects Myocardial Stunning: • Reperfusion to myocardium à Delay in return of complete normal function Myocardial Hibernation: • Chronic ischemic myocardium à Left ventricular adaptation à Ischemic cardiomyopathy, LV systolic dysfunction Reperfusion Injury: • Reperfusion to myocardium à Oxidative and inflammatory damage to myocardium

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Cardiology: Myocardial Infarction

https://commons.wikimedia.org/wiki/File:Histopathology_of_myofiber_waviness_in_myocardial_infarction.jpg https://commons.wikimedia.org/wiki/File:Glanzstreifen.jpg

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https://commons.wikimedia.org/wiki/File:Histopathology_of_myocardial_infarction_with_karyorrhexis_and_few_lymphocytes.jpg

• •

•

•

Acute Phase (First 24 hours): • Gross exam: No abnormal changes up to about 12 hours • Histopathology: ↑ Neutrophils, bordering wavy fibers, cytoplasm hypereosinophilia, pyknotic nuclei Inflammatory Phase (Hours-Days): • ↑ Inflammatory response • Macrophages and neutrophils à Phagocytose necrotic tissue, release cytokines à Stimulate tissue proliferation • Histopathology: Coagulative necrosis, loss of nuclei, neutrophil and macrophages present Proliferative Phase (Days-Weeks): • ↓ Inflammatory response (TGF-β) • Fibroblasts à Collagen deposited (Type I and III) à ↓ Electrical conductivity through areas of fibrosis • Histopathology: Granulation tissue, collagen deposition Remodeling Phase (Weeks-Months): • ↓ Inflammatory response (TGF-β) • Matrix metalloproteinases à Collagen crosslinking à Scar tissue • Histopathology: Scar tissue, ↑ Collagen, ↓ Cellularity

https://commons.wikimedia.org/wiki/File:Histopathol ogy_of_fibroblast_proliferation_and_early_collagen _deposition_in_myocardial_infarction.jpg https://commons.wikimedia.org/wiki/File:Histopatho logy_of_dense_fibrous_scar_replacing_myocyte_l oss_in_myocardial_infarction.jpg

Cardiology: Myocardial Infarction

https://commons.wikimedia.org/wiki/File:Heart_pseudoaneurysm_a4c.jpg https://commons.wikimedia.org/wiki/File:Heart_lv_aneurysm_4c.jpg

•

•

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•

Acute Phase (First 24 hours): • Ventricular arrhythmia à Sudden cardiac death • Papillary muscle rupture (posteromedial papillary muscle à posterior descending artery occlusion) à Acute mitral regurgitation • Interventricular septal rupture à Ventricular septal defect Inflammatory Phase (Hours-Days): • Peri-infarction pericarditis à Inflammatory response near infarct à Diffuse STE, pleuritic chest pain • Papillary muscle rupture • Interventricular septal rupture Proliferative Phase (Days-Weeks): • Left ventricular pseudoaneurysm (right coronary artery occlusion is classic) à Mural thrombus • Left ventricular free wall rupture à Cardiac tamponade Remodeling Phase (Weeks-Months): • Left ventricular aneurysm à Persistent STE and TWI, ↑ Risk of free wall rupture and mural thrombus • Dressler syndrome à Antibodies against myocardium à Diffuse STE, pleuritic chest pain • Reinfarction risk ↑ over time

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Cardiology: Myocardial Infarction

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https://commons.wikimedia.org/wiki/File:EKG_leads.png https://commons.wikimedia.org/wiki/File:Blausen_0256_CoronaryArteries_02.png

https://commons.wikimedia.org/wiki/File:Left_bundle_branch_block_ECG_characteristics.svg

•

•

Infarct Age: • Hyperacute à Peaked T-waves • Acute à ST-elevations, new LBBB • Chronic (Previous MI) à Deep Q-waves, T-wave inversions ST elevations: • Peaked T-waves (initial) • ST-elevation in 2 contiguous leads • Reciprocal ST-depression

https://commons.wikimedia.org/wiki/File:EKG_leads.png

Location

Leads Affected

Artery

Lateral

I, aVL, V5-V6

Left lateral circumflex

Anterior

V1-V4

Left anterior descending

Anterolateral

I, aVL, V1-V6

Left main

Inferior

II, III, aVF

Right coronary

Posterior

ST depression and tall R waves in V1-V3 ST elevation in V7-V9

Posterior descending artery

Cardiology: Myocardial Infarction

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Location AfraTafreeh.com

Leads Affected

Artery

Lateral

I, aVL, V5-V6

Left lateral circumflex

Anterior

V1-V4

Left anterior descending

Anterolateral

I, aVL, V1-V6

Left main

Inferior

II, III, aVF

Right coronary

Posterior

ST depression and tall R waves in V1-V3 ST elevation in V7-V9

Posterior descending artery

https://commons.wikimedia.org/wiki/File:ECG_001.jpg

Cardiology: Myocardial Infarction

AfraTafreeh.com https://commons.wikimedia.org/wiki/File:AMI_bloodtests_engl.png

• •

Troponin • Peak: 12-48 hours • Return to normal: 5-14 days CK-MB • Peak: 24 hours • Return to normal: 48-72 hours • Potential marker for re-infarction

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Cardiology: Myocardial Infarction

Bootcamp.com https://commons.wikimedia.org/wiki/File:HWI_PTCA.jpg

• • • • • •

Statin: • Atorvastatin, Rosuvastatin: HMG-CoA reductase inhibitor à ↓ LDL, stabilize plaque, ↓ inflammation Antiplatelet: • Aspirin: Inhibition of cyclooxygenase à Irreversible inhibition of platelet aggregation • Clopidogrel: P2Y12 inhibitor à Irreversible inhibition of platelet aggregation Glycoprotein IIb/IIIa Inhibitor:: • Abciximab, Eptifibatide, Tirofiban: Inhibition of fibrinogen binding to platelets • Can be utilized in preparation for PCI Anticoagulation: • Heparin: ↑ activity of antithrombin III à ↓ thrombin and factor Xa Thrombolytics (Fibrinolytics): • Alteplase, tenecteplase (tPA) à ↑ Plasmin à Fibrin thrombus breakdown • ↑ Risk of bleeding Percutaneous Coronary Intervention (PCI): • Preferred for revascularization in STEMI • Femoral or radial artery access site • Balloon dilation over atheromatous plaque +/- stent placement • Door-to-balloon time 90 minutes or less • PCI not typically performed when >120 minutes from first medical contact

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A 63-year-old male with a past medical history of hyperlipidemia and type II diabetes mellitus presents to the emergency department with progressively worsening retrosternal chest discomfort and dyspnea for the past week. He states that he frequently wakes up in the middle of the night due to the pain. The patient was recently admitted for percutaneous coronary intervention for a complete obstruction of the right coronary artery approximately 1 week earlier. On physical examination blood pressure is 156/88 mmHg, heart rate is 84 beats/min, respiratory rate is 12/min, and oxygen saturation is 97% on room air. Electrocardiogram reveals deep Q waves in leads II, III, and aVF. Chest X-ray reveals cardiomegaly with clear lung fields. Echocardiography is shown below. Doppler flow reveals the presence of bidirectional turbulent flow into an ominous “mushroom cloud”. Which of the following best describes the cause of this patient’s presentation?

⚪ A. Localized thinning and dyskinesia of myocardium ⚪ B. Contained left ventricular free wall rupture ⚪ C. Open left ventricular free wall rupture into pericardium ⚪ D. Interventricular septal wall rupture ⚪ E. Posteromedial papillary muscle rupture

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https://commons.wikimedia.org/wiki/File:Mushroom-cloud-a-giant-left-ventricularpseudoaneurysm-after-a-myocardial-infarction-due-to-1476-7120-7-36-S2.ogv

OUTLINE 1.

Peripheral Venous Disease

● A. Lower Extremity Veins ● B. Chronic Venous Insufficiency ● C. Deep Vein Thrombosis ● D. Migratory Superficial Thrombophlebitis 2. Peripheral Artery Disease ● A. Lower Extremity Arteries ● B. Peripheral Arterial Disease ● C. Leriche Syndrome ● D. Ankle-Brachial Index 3. Lower Extremity Ulcer Comparison ● A. Venous Ulcer ● B. Arterial Ulcer ● C. Neuropathic Ulcer

Cardiology: Peripheral Venous and Arterial Disease AfraTafreeh.com

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Cardiology: Peripheral Venous and Arterial Disease

Bootcamp.com https://commons.wikimedia.org/wiki/File:Leg_Before_1.jpg

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Lower Extremity Veins Affected in PVD • Superficial: Great saphenous, small saphenous veins • Deep: Anterior, Posterior tibial + Fibular veins à Popliteal vein à Femoral vein à External iliac vein Chronic Venous Insufficiency: • Incompetent venous valves à Blood remains in veins à ↑ Venous hydrostatic pressure • Tortuous dilated superficial veins (Varicose veins) • Presentation: Lower extremity pain, skin pigmentation of medial malleolus, varicose veins • Improves with ↓ venous hydrostatic pressure (raising leg) • Improves with ambulation • Venous Duplex U/S: Venous reflux • Symptomatic Management: Compression stocks, leg elevation • Definitive Management: Vein ablation • Complications: Venous ulcer à Proximal to ankle, +/- infection • Complications: Stasis dermatitis, chronic edema Deep Vein Thrombosis • Virchow’s Triad: Venous stasis, damage, hypercoagulability • Unilateral (classically) • Homan’s sign • Erythematous swelling • D-dimer: Negative test à Rules out (SN-OUT) • Positive D-dimer does not diagnose a DVT! • Venous Duplex U/S: Incompressible, luminal mass, ↓ flow • Management: Anticoagulation, IVC filter • Complication: Pulmonary embolus Migratory Superficial Thrombophlebitis • Trousseau syndrome • Classically associated with malignancy • Hypercoagulability à Superficial venous thrombus • Recurring at multiple sites https://commons.wikimedia.org/wiki/File:Chronicvenousinsufficiency.jpg

https://commons.wikimedia.org/wiki/File:2136ab_Lower_Limb_Veins_Anterior_Posterior.jpg

Cardiology: Peripheral Venous and Arterial Disease

Bootcamp.com https://commons.wikimedia.org/wiki/File:GangreneFoot.JPG

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Lower Extremity Arteries Affected in PAD • Femoral artery à Popliteal artery à Anterior, Posterior tibial and Fibular arteries Peripheral Arterial Disease: • Atherosclerosis à ↓ Arterial perfusionà ↑ Venous hydrostatic pressure • Smoking is primary risk factor • Presentation: Intermittent claudication (calf is classic) à Worse with exertion, improves with rest • Weakened pulses (femoral, posterior tibial, dorsalis pedis) • Absent hair growth, cyanosis peripheral to lesion • Improves with ↑ arterial hydrostatic pressure (lowering leg) • Worsened with ambulation and leg elevation (elevation pallor) • Duplex U/S: Venous reflux • Management: ↓ Modifiable risk factors (smoking), graded exercise therapy, cilostazol • Definitive Management: Vein ablation • Complications: Arterial ulcer à Pressure points, lateral malleolus is classic • Complications: Distal gangrene Leriche Syndrome: • Triad: Bilateral hip/thigh claudication, erectile dysfunction, diminished femoral pulses Ankle-Brachial Index: • Systolic Ankle BP / Systolic Brachial BP (some stipulations) • < 0.9 suggests PAD

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https://commons.wikimedia.org/wiki/File:Blausen_0607_LegArteries.png

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Cardiology: Peripheral Venous and Arterial Disease

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Type

Location

Exacerbating Pain

Improving Pain

Other

Venous

Proximal to ankle

At rest, gravity dependent

Activity, leg raise

Varicose veins Peripheral edema

Arterial

Pressure points

Activity, leg raise

At rest, gravity dependent

ABI < 0.9 ↓ DP and PT pulses Cyanosis, absent hair peripheral to lesion

Neuropathic

Plantar surface of foot

Absent pain

Absent pain

Diabetic peripheral neuropathy Diminished S1 reflex

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Item 1 of 1 Question ID: 0054

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A 65-year-old female with a past medical history of morbid obesity, chronic systolic heart failure, and poorly controlled hypertension who presents to her primary care provider for a “sore above her foot”. The patient states that she noticed a small wound above her left ankle two months earlier that has been progressively growing in size. She also reports noticing some yellow-gray color fluid draining from the wound this morning. The patient mentions that she prefers to keep moving since the pain is worse when resting. The patient has a 1cm superficial irregularly-shaped ulcer located on the medial lower leg approximately 10cm above the medial malleolus. The wound is actively draining purulent exudate. Peripherally, the patient has evidence of brown discoloration leading up to the pretibial surface of the leg. Both lower extremities demonstrate 2+ pitting edema up to the knee. The patient is tender to light palpation in the area surrounding the lesion. Which of the following best describes the mechanistic etiology of this patient’s ulcer?

⚪ A. Sensory neuropathy ⚪ B. Decreased arterial luminal diameter ⚪ C. Peri-local mechanical stress ⚪ D. Infection of glandular tissue ⚪ E. Elevated venous hydrostatic pressure

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AfraTafreeh.com OUTLINE

1. Overview

Cardiology: Hypertension

2. Essential Hypertension ● A. Pathophysiology ● B. Risk Factors ● C. Screening 3. Hypertension Variants ● A. White Coat Hypertension ● B. Isolated Systolic Hypertension ● C. Hypertensive Urgency ● D. Hypertensive Emergency 4. Hypertensive End-Organ Disease ● A. Cardiovascular ● B. Neurovascular ● C. Renovascular 5. Secondary Hypertension ● A. Aortic Coarctation ● B. Cushing Syndrome ● C. Hyperaldosteronism ● D. Renal Artery Stenosis ● E. Obstructive Sleep Apnea ● F. Pheochromocytoma ● G. Hyperthyroidism

6. ● ● ● ● ● ● ●

Antihypertensives A. ACE Inhibitors B. Angiotensin Receptor Blockers C. Calcium Channel Blockers D. Thiazide Diuretics E. β-blockers F. Nitrates G. Hydralazine, Minoxidil

Cardiology: Hypertension

• • •

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Definition: • JNC 8: SBP ≥ 140 mmHg and/or DBP ≥ 90mmHg Essential Hypertension: • Majority of cases • Idiopathic Secondary Hypertension • Underlying etiology à treat cause, treat HTN • Uncommon

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Cardiology: Hypertension

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•

•

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Pathophysiology: • MAP = CO x TPR = (SV x HR) x TPR • SV ~ Preload à ↑ Serum Na+ • HR à Anxiety/stress • TPR à Atherosclerosis Risk Factors: • Older age, ethnicity • Obesity • Diabetes Mellitus • Tobacco use • High sodium diet Screening: • >40 years old or ↑ risk à Screen annually (USPSTF) • Generally asymptomatic

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Cardiology: Hypertension

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• •

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White Coat Hypertension: • ↑ BP in clinical setting • Normal BP at home Isolated Systolic Hypertension • Elderly patient • Normal DBP • ↑ Arterial stiffness, ↓ arterial compliance Hypertensive Urgency • ≥180/120 mmHg (no evidence of end-organ damage) Hypertensive Emergency • ≥ 180/120 mmHg + evidence of end-organ damage • Rx: Labetalol • Rx: Nitrates (Angina) • Rx: Fenoldopam (AKI)

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Cardiology: Hypertension

AfraTafreeh.com https://commons.wikimedia.org/wiki/File:Papilledema.jpg https://commons.wikimedia.org/wiki/File:Hypertensiveretinopathy.jpg

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Cardiovascular: • Concentric LVH à Diastolic heart failure (↑ β-myosin heavy chain) • Coronary artery disease • Aortic dissection Neurovascular: • Lacunar CVA (classic) • Retinopathy • Diabetes Mellitus • Tobacco use • High sodium diet Renovascular: • Chronic kidney disease • Hyperplastic arteriosclerosis à “onion skin” appearance

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Cardiology: Hypertension

• • • •

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Aortic Coarctation: • Asymmetric BP between arms and legs • Brachial-femoral pulse delay Cushing Syndrome: • Iatrogenic common cause • Central obesity, proximal muscle weakness, hirsutism, abdominal striae, “moon facies” Hyperaldosteronism • Metabolic alkalosis, hypokalemia +/- hypernatremia Renal Artery Stenosis • Young patient à Fibromuscular dysplasia • Older patient à Atherosclerosis • Unilateral à Hypoperfusion à Atrophy of affected kidney (Contralateral renal hypertensive nephrosclerosis) Obstructive Sleep Apnea: • Snoring, intermittent period of apnea reported by patient partner • Daytime sleepiness • Rx: CPAP qhs Pheochromocytoma: • Episodes of ↑ sympathetic response • Serum metanephrines à 24h urinary metanephrines • Rx: Irreversible non-selective ⍺-block à β-blocker à Surgery Hyperthyroidism: • ↓ TSH, ↑ free T4 • Pretibial myxedema, heat intolerance, ↑ pulse pressure, exophthalmos, goiter

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•

•

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https://commons.wikimedia.org/wiki/File:%22Onion-skin%22_renal_arteriole.jpg

Cardiology: Hypertension

•

•

•

•

•

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•

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ACE Inhibitors (Lisinopril, Captopril, Enalapril, -pril) • Inhibition of ACE à ↑ angiotensin I and renin, ↓ angiotensin II • Use: Hypertension, Nephroprotective effects (Diabetes), Cardioprotective effects (Heart failure) • Adverse Effect: Dry cough, hyperkalemia, angioedema, teratogenic Angiotensin Receptor Blockers (ARBs) (Valsartan, Losartan, -sartan) • Receptor blockade of angiotensin II type 1 receptor • Use: Hypertension, Nephroprotective effects (Diabetes), Cardioprotective effects (Heart failure) • Adverse Effect: Hyperkalemia, teratogenic

Dihydropyridine Calcium Channel Blockers (Amlodipine, Nifedipine) • Inhibition of L-type calcium channels in vascular smooth muscle • Adverse Effect: Peripheral edema Thiazide Diuretic (Hydrochlorothiazide, Chlorthalidone) • Inhibition of Na/Cl transporter in distal tubule • Adverse Effect: Hyperglycemia, hyperlipidemia, hyperuricemia, hypokalemia, hyponatremia β-blockers • Labetalol: Blockade of β1, β2, ⍺1 à Hypertensive emergency • Metoprolol: Blockade of β1 receptorsà Added for heart failure, coronary artery disease, atrial fibrillation • Adverse Effect: Bradycardia Nitrates (Sodium nitroprusside) • ↑ cGMP à ↓ Intracellular Ca2+ à Venous and arterial vasodilation (Nitroglycerin primarily venous) • Adverse Effect: Reflex tachycardia, Monday’s Disease, cyanide toxicity (chronic use), avoid with PDE-5 inhibitors Hydralazine, Minoxidil • Arterial vasodilation • Hydralazine used in pregnancy • Adverse Effect: Reflex tachycardia, peripheral edema, DIL (Hydralazine)

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Item 1 of 1 Question ID: 0055

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A 41-year-old male with a past medical history of intermittent asthma as an adolescent presents to his primary care physician stating that he has worsening of his panic attacks over the past two months. He reports episodes of diffuse sweating and palpitations that last approximately 10 minutes on average with some instances lasting up to one hour. The patient reports increased frequency of symptoms when he is active or exercising. He also states that he has had unrelenting headaches when the episodes are at their worst. The patient is currently not taking any medications and denies any alcohol or recreational drug use. Vital signs reveal a temperature of 98F (36.7C), blood pressure of 154/92 mmHg, heart rate of 112/min, and a respiratory rate of 18/min. Physical examination reveals tachycardia with a regular rhythm and is otherwise relatively unremarkable. An electrocardiogram reveals sinus tachycardia. A detailed workup is performed revealing a large left-sided adrenal mass. A decision is made to proceed with laparoscopic tumor resection. Prior to the procedure, two antihypertensive medications were given. Which of the following was most likely the first of these medications administered to the patient?

⚪ A. Nephron inhibitor of Na/K/Cl cotransporters ⚪ B. Nephron inhibitor of Na/Cl cotransporters ⚪ C. Nonselective ⍺-blocker ⚪ D. Nonselective β-blocker ⚪ E. Cardioselective β-blocker

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AfraTafreeh.com OUTLINE

1. Acute Pericarditis

Cardiology: Pericardial Disease

● A. Pathogenesis ● B. Etiology ● C. Presentation ● D. Diagnostics ● E. Management ● F. Complications 2. Constrictive Pericarditis ● A. Pathogenesis ● B. Etiology ● C. Presentation ● D. Diagnostics ● E. Management 3. Pericardial Effusion ● A. Pathogenesis ● B. Etiology ● C. Diagnostics ● D. Management 4. Cardiac Tamponade ● A. Pathogenesis ● B. Etiology ● C. Presentation ● D. Diagnostics ● E. Management ● F. Complication

Cardiology: Pericardial Disease

• •

•

•

•

•

https://commons.wikimedia.org/wiki/File:PericarditisECG.JPG

Pathogenesis: • Pericardial inflammation Etiology: • Viral à Coxsackie B virus (classic) • Bacterial • Myocardial infarction à Peri-infarction pericarditis, Dressler syndrome • Post-operatively, Blunt or penetrating trauma • Uremia • Radiation • Autoimmune Presentation: • Pleuritic, sharp, retrosternal chest pain • Improves with leaning forward • Worsens with lying down • +/- Fever • Friction rub Diagnostics: • ECG: Diffuse ST-elevations, PR-depressions • CXR: Non-specific, enlarged silhouette • Echocardiography: Non-specific, +/- pericardial effusion Management: • Treat underlying etiology • Conservative • NSAIDs symptomatic control and preventative Complications: • Constrictive pericarditis • Pericardial effusion à Tamponade

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Cardiology: Pericardial Disease

AfraTafreeh.com https://intjem.biomedcentral.com/articles/10.1186/1865-1380-5-37/figures/1

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Pathogenesis: • Fibrous pericardium à Restricted right ventricular filling Etiology: • Chronic Pericarditis • Radiation • Tuberculosis Presentation: • Jugular venous distension • Kussmaul sign • Hepatomegaly • Peripheral edema • Pericardial knock • Pulsus paradoxus Diagnostics: • ECG: Non-specific, low voltage • CXR: Thickening of pericardium, calcifications • Echocardiography: Thickening of pericardium Management: • Variable depending on severity • Pericardiectomy

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Cardiology: Pericardial Disease

Bootcamp.com https://commons.wikimedia.org/wiki/File:Electrical_Alternans.JPG https://commons.wikimedia.org/wiki/File:PericardialeffusionUS.PNG

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•

•

Pathogenesis: • Fluid accumulation within pericardial space Etiology: • Acute pericarditis • Malignancy Presentation: • Incidental finding (common) • Orthopnea • Chest pain Diagnostics: • CXR: Water-bottle sign (if massive) • ECG: Electrical alternans, low voltage • Echocardiography: Pericardial fluid Management: • Conservative vs Pericardiocentesis

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https://commons.wikimedia.org/wiki/File:Pericarditis_can_progress_to_pericardial_effusion_and_eventually_cardiac_tamponade.jpg https://commons.wikimedia.org/wiki/File:Massivepericarialeffusion.png

Cardiology: Pericardial Disease

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•

• • •

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Pathogenesis: • Rapid ↑ in pericardial effusion à ↑↑↑ Pericardial pressure à Chamber compression Etiology: • Aortic dissection • Ventricular free wall rupture (Complication of MI) • Post-operative, trauma • Worsening of pericardial effusion Presentation: • Beck’s Triad: Hypotension, ↑ JVP, Muffled heart sounds • Pulsus paradoxus • Tachycardia Diagnostics: • Echocardiography: Collapsing cardiac chambers • Similar EDP throughout cardiac chambers Management: • Pericardiocentesis (generally) • Pericardial window (hemopericardium) Complication: • Obstructive shock à Cardiac arrest à PEA

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Item 1 of 1 Question ID: 0056

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A 67-year-old female presents to the emergency department with shortness of breath. She states that her symptoms have progressively been worsening and are most notable when climbing stairs in her home. She has a 50-pack year smoking history and a history of non-metastatic esophageal carcinoma. The patient has completed a course of chemoradiation therapy 6 months earlier. She denies any family history of heart disease. Vital signs reveal a temperature of 98.7F (37.1C), blood pressure of 94/58 mmHg, heart rate 102/min, and a respiratory rate of 14/min. Jugular venous distension and hepatomegaly are observed. Lung sounds are vesicular in nature. Systolic blood pressure measured in deep inspiration is 76 mmHg. Chest X-ray is shown. Which of the following findings would be most consistent with the jugular venous tracing observed in this patient?

⚪ A. Prominent x and y descent ⚪ B. Prominent v waves ⚪ C. Cannon a waves ⚪ D. Absent a waves ⚪ E. Absent y descent

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https://commons.wikimedia.org/wiki/File:33-01-Pericarditis_calcarea_pa.png

AfraTafreeh.com OUTLINE 1.

Cardiology: Shock

Overview

● A. General Principles ● B. Management 2. Hypovolemic Shock ● A. Pathophysiology ● B. Etiology ● C. Hemorrhagic Shock ● E. Management 3. Cardiogenic Shock ● A. Pathophysiology ● B. Etiology ● C. Presentation 4. Obstructive Shock ● A. Pathophysiology ● B. Etiology ● C. Presentation 5. Septic Shock ● A. Pathophysiology ● B. Etiology ● C. Presentation 6. Anaphylactic Shock ● A. Pathophysiology ● B. Etiology ● C. Presentation 7. Neurogenic Shock ● A. Pathophysiology ● B. Etiology ● C. Presentation

Cardiology: Shock

• •

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General: • ↓ Organ perfusion à ↑ Lactic acidosis à ↑ AG-metabolic acidosis • ↑ Ventilation à ↓ PaCO2 à Compensatory respiratory alkalosis Management: • Variable for each disease process • Treat underlying pathology if possible • IVF +/- blood products (when applicable) • Adrenergic agonists (vasopressors) à Phenylephrine, norepinephrine Shock

Disturbance

Compensation

CVP

PCWP

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Hypovolemic

↓ Circulating volume

↑ HR, ↑ TPR

Cardiogenic

↓ LV function

↑ HR, ↑ TPR

↓ Forward flow

Septic

Stroke Volume (forward)

Heart Rate

TPR

↓

↓

↓

↑

↑

↑

↑

↓

↑

↑

↑ HR, ↑ TPR

↑

↑/↓

↓

↑

↑

Systemic vasodilation

↑ HR, ↑ SV

↓

↓

↑

↑

↓

Anaphylactic

Systemic vasodilation

↑ HR, ↑ SV

↓

↓

↑

↑

↓

Neurogenic

Systemic vasodilation

Minimal

↓

↓

---/↓

---/↓

↓

Obstructive

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Cardiology: Shock

• • • • •

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Pathophysiology: • Disturbance: ↓ Circulating volume à ↓ LVEDV à ↓ SV à ↓ CO • Compensation: ↑ HR, ↑ TPR Etiology: • Hemorrhage à Traumatic injury, UGIB • Severe dehydration à Diarrhea, burn, iatrogenic Hemorrhagic Shock Classification: • Tachycardia (early), hypotension (later) • ↑ HR, ↓ MAP, ↑ RR, ↓ UOP Presentation: • Cold, clammy skin • Low volume status à ↓ skin turgor, dry oral mucosa, ↓ JVP, pre-renal azotemia (BUN/Cr > 20:1) Management: • Blood pressure support • Hemorrhagic: Eliminate sources of bleeding, blood products, crystalloid solutions

Shock Hypovolemic

Disturbance

↓ Circulating volume

Compensation

↑ HR, ↑ TPR

CVP

PCWP

↓

Stroke Volume (forward)

↓

↓

Heart Rate

↑

TPR

↑

Cardiology: Shock

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•

•

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Pathophysiology: • Disturbance: LV failure à ↓ Contractility, ↓ SV à ↓ CO • Compensation: ↑ HR, ↑ TPR Etiology: • Cardiovascular disease à MI (MCC), HF, arrhythmias • Trauma • Iatrogenic Presentation: • Cold, clammy skin • Chest pain, dyspnea, palpitations • High volume status (Low ECV) à ↑ JVP Management: • Blood pressure support • Inotropic agent when applicable • MI à Revascularization, thrombolytic • Arrhythmia à Antiarrhythmic

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Shock Cardiogenic

Disturbance ↓ LV function

Compensation ↑ HR, ↑ TPR

CVP

PCWP

↑

Stroke Volume (forward)

↑

↓

Heart Rate

↑

TPR

↑

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Cardiology: Shock

• •

•

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Pathophysiology: • Disturbance: Obstruction to forward flow à ↓ CO • Compensation: ↑ HR, ↑ TPR Etiology: • Pulmonary disease: Tension pneumothorax, PHTN, PE • Pericardial disease: Cardiac tamponade, constrictive pericarditis • Myocardial disease: Restrictive cardiomyopathy • Aortic disease: Aortic dissection, aortic stenosis Presentation: • Cold, clammy skin • High volume status (Low ECV) à ↑ JVP • Correlate with specific etiology presentation Shock Obstructive

Disturbance

↓ Forward flow

Compensation

↑ HR, ↑ TPR

CVP

PCWP

↑

↑/↓

Stroke Volume (forward)

↓

Heart Rate

↑

TPR

↑

Cardiology: Shock

•

• •

Pathophysiology: • Disturbance: Systemic vasodilation à ↓ TPR • Initial Compensation: ↑ HR, ↑ SV à ↑ CO • Late Stage: ↓ Circulating volume à à ↓ LVEDV à ↓ SV à ↓ CO Etiology: • Sepsis, inflammatory response Presentation: • Warm, dry skin (early) à Cold, clammy skin (late)

• •

•

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↑ Mixed venous O2 saturation Correlate with specific etiology presentation

Management: • Blood pressure support • Antibiotics

Shock

Disturbance

Septic

Systemic vasodilation

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Compensation

↑ HR, ↑ SV

CVP

PCWP

↓

Stroke Volume (forward)

↓

↑

Heart Rate

↑

TPR

↓

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Cardiology: Shock

•

• • •

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Pathophysiology: • Disturbance: Mast cell degranulation à ↑ Histamine à ↓ TPR • Initial Compensation: ↑ HR, ↑ SV à ↑ CO • Late Stage: ↓ Circulating volume à à ↓ LVEDV à ↓ SV à ↓ CO Etiology: • Type I hypersensitivity Presentation: • Warm, dry skin (early) à Cold, clammy skin (late) Management: • Blood pressure support • Epinephrine

Shock Anaphylactic

Disturbance

Systemic vasodilation

Compensation

↑ HR, ↑ SV

CVP

PCWP

↓

Stroke Volume (forward)

↓

↑

Heart Rate

↑

TPR

↓

Cardiology: Shock

• • • • •

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Pathophysiology: • Disturbance: ↓ SNS à ↓ TPR • No compensation in HR or contractility Etiology: • Autonomic dysregulation Presentation: • Warm, dry skin (early) à Cold, clammy skin (late) • Hypotension in setting of bradycardia Differential: • β-blocker overdose à Glucagon Management: • Blood pressure support • Atropine

Shock Neurogenic

Disturbance Systemic vasodilation

Compensation

Minimal

AfraTafreeh.com

CVP

PCWP

↓

Stroke Volume (forward)

↓

---/↓

Heart Rate

---/↓

TPR

↓

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Cardiology: Shock

Shock

Disturbance

Compensation

Hypovolemic

↓ Circulating volume

↑ HR, ↑ TPR

Cardiogenic

↓ LV function

↑ HR, ↑ TPR

↓ Forward flow

Septic

CVP

PCWP

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Stroke Volume (forward)

Heart Rate

TPR

↓

↓

↓

↑

↑

↑

↑

↓

↑

↑

↑ HR, ↑ TPR

↑

↑/↓

↓

↑

↑

Systemic vasodilation

↑ HR, ↑ SV

↓

↓

↑

↑

↓

Anaphylactic

Systemic vasodilation

↑ HR, ↑ SV

↓

↓

↑

↑

↓

Neurogenic

Systemic vasodilation

Minimal

↓

↓

---/↓

---/↓

↓

Obstructive

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Item 1 of 1 Question ID: 0057

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A 57-year-old male is sent to the emergency department from his cardiologist’s office for severe chest pain and diaphoresis. He is a former smoker and has a history of poorly controlled type II diabetes mellitus, dyslipidemia, and symptomatic peripheral artery disease. ECG reveals ST-segment elevation in the anterolateral leads. The patient undergoes revascularization without complication. The patient is subsequently discharged and returns one week later with dyspnea and pre-syncope. Blood pressure is 84/58mmHg, heart rate 110/min, respiratory rate is 20/min. Heart sounds are difficult to auscultate. Hepatomegaly and modest jugular venous distention are appreciated. Low voltage R waves are observed on ECG with alternating amplitudes. Chest X-ray is shown below. Which of the following pathophysiologic changes most correlate with this patient’s current presentation?

Total Peripheral AfraTafreeh.com Resistance

Central Venous Pressure

Pulmonary Capillary Wedge Pressure

Cardiac Output

⚪A

↓

↓

↑

↓

⚪B

↓

↓

↓

↓

⚪C

↓

↓

↓

↑

⚪D

↑

↑

↓

↑

⚪E

↑

↓

↓

↑

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